Biological Procedures Online最新文献

{"title":"Molecular regulatory network of glycolytic reprogramming in hepatocellular carcinoma and its clinical implications.","authors":"Hengzhou Zhu, Jiahui Li, Jiaying Zhang, Dong Niu, Weiwang Zheng, Chunhui Jin","doi":"10.1186/s12575-025-00318-w","DOIUrl":"10.1186/s12575-025-00318-w","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) ranks among the most prevalent malignant tumors worldwide, exhibiting persistently high incidence and mortality rates. Metabolic reprogramming, particularly the 'Warburg effect' characterized by aberrantly enhanced glycolysis, serves as a hallmark feature of HCC and various other malignancies. Even under oxygen-sufficient conditions, tumor cells preferentially utilize the glycolytic pathway to convert glucose into lactate. This metabolic mode not only supplies essential energy (ATP) for rapid tumor cell proliferation but, more critically, provides key intermediate metabolites for synthesizing macromolecules such as nucleic acids, lipids, and amino acids. It concurrently regulates the pH and redox status of the tumor microenvironment, thereby robustly supporting tumor growth, invasion, and metastasis. Recent years have witnessed significant advances in research on glycolytic regulatory mechanisms in HCC, revealing an exceptionally complex regulatory network composed of diverse molecules and signaling pathways. This review aims to systematically organize and elucidate the multi-layered molecular mechanisms regulating glycolytic reprogramming in HCC. We will comprehensively examine the multidimensional regulation of key enzymes and glucose transporters within the glycolytic pathway, encompassing transcriptional control, post-translational modifications, and other regulatory layers; We will conduct an in-depth analysis of the central role played by non-coding RNAs (ncRNAs)-including long non-coding RNAs (lncRNAs), circular RNAs (circRNAs), and microRNAs (miRNAs)-within the glycolytic regulatory network of HCC; Elucidate how classical signaling pathways and key transcription factors synergistically interact to precisely regulate the glycolytic process; Analyze how post-translational modifications fine-tune the activity of glycolytic enzymes; And discuss how various components within the tumor microenvironment and intercellular communication mechanisms reshape the metabolic phenotypes of HCC. Furthermore, this review summarizes the clinical application value of positron emission tomography (PET) technology based on glycolytic activity in the diagnosis, staging, and prognostic evaluation of HCC. Through a comprehensive elucidation of these complex regulatory networks, this work aims to enhance comprehension of HCC metabolic characteristics and provide a theoretical foundation for exploring novel therapeutic targets and clinical strategies.</p>","PeriodicalId":8960,"journal":{"name":"Biological Procedures Online","volume":" ","pages":"51"},"PeriodicalIF":4.3,"publicationDate":"2025-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12751871/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145809372","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Paris polyphylla enhances the anti-metastatic efficacy of maimendong decoction against lung cancer.","authors":"Zhipeng Zhang, Jiaxuan Li, Wenfei Shi, Zujun Que, Wang Yao, Jialiang Yao, Wenji Shangguan, Weikang Zhu, Likun Liu, Jianhui Tian","doi":"10.1186/s12575-025-00317-x","DOIUrl":"10.1186/s12575-025-00317-x","url":null,"abstract":"<p><p>BACKGROUND: Maimendong decoction (MMDD), a classic traditional Chinese medicine (TCM) formula prescribed for ‘lung atrophy’, has demonstrated efficacy against various pulmonary disorders. Our prior research confirmed that MMDD inhibit lung cancer metastasis by modulating natural killer (NK) cells. Paris polyphylla (P.P), a TCM herb with known anti-tumor properties, is often incorporated into classic formulas to enhance therapeutic outcomes. This study aimed to boost the anti-metastatic efficacy of MMDD against lung cancer by incorporating Paris polyphylla (Chonglou) and to investigate the underlying mechanisms. METHODS: The Modified Maimendong Decoction (MMDD + P.P) Was Prepared by Adding 9–18 g of Paris polyphylla. Its Effects on the proliferation, migration, and Apoptosis of CTC-TJH-01 and LLC Cells Were Assessed Using CCK-8, Transwell, and Annexin V-FITC/PI Flow Cytometry assays. Apoptosis-related Proteins Were Analyzed by Western blot. A Tail Vein injection-induced Lung Metastasis Model in C57BL/6 Mice Was Established To Evaluate the Effects of MMDD + P.P, both Alone and in Combination with an anti-PD-1 antibody, on Metastasis Flow cytometry was used to profile T cell and NK cell populations in peripheral blood. Histological and molecular analyses of metastatic tissues were performed using H&E staining, immunohistochemistry (for Ki-67 and cleaved caspase-3), and immunofluorescence (for CD8+ T cell and NK cell infiltration). RESULTS: Compared to MMDD alone, MMDD + P.P (18 g) significantly inhibited proliferation and migration, and induced apoptosis in both CTC-TJH-01 and LLC cells. These effects were associated with the upregulation of pro-apoptotic proteins (cleaved caspase-3, BAX, cleaved PARP) and downregulation of anti-apoptotic proteins (BCL-2, Survivin). In vivo, while both MMDD and MMDD + P.P reduced the number of lung metastatic nodules, MMDD + P.P (18 g) was uniquely effective in significantly reducing overall tumor burden, which correlated with decreased Ki-67 and increased cleaved caspase-3 in metastatic foci. Furthermore, MMDD + P.P (18 g) significantly increased the proportions and tumor-infiltration of NK cells and CD8+ T cells. It also synergized with anti-PD-1 therapy, enhancing its anti-metastatic effect and boosting the expression of cytotoxic markers (CD107a, perforin, granzyme B) and TNF-α in CD8+ T cells. CONCLUSION: Incorporating Paris polyphylla into MMDD enhances its anti-metastatic efficacy through a dual mechanism: directly inducing apoptosis in lung cancer cells and amplifying anti-tumor immunity by increasing the abundance and cytotoxic function of CD8+ T cells. The synergy between MMDD + P.P and anti-PD-1 antibody therapy highlights the potential of this modified TCM formula as a promising adjunctive treatment for inhibiting lung cancer metastasis. </p>","PeriodicalId":8960,"journal":{"name":"Biological Procedures Online","volume":" ","pages":"50"},"PeriodicalIF":4.9,"publicationDate":"2025-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12751362/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145809369","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Network Pharmacology and Experimental Validation Reveal Aidi Injection Suppresses Prostate Cancer via EGFR Inhibition and STAT3-Mediated Apoptosis.","authors":"Ganhua You, Chen Qian, Xiaoyue Chen, Qunying An, Jukun Song, Yuehai Xiao","doi":"10.1186/s12575-025-00299-w","DOIUrl":"10.1186/s12575-025-00299-w","url":null,"abstract":"<p><strong>Background: </strong>Prostate cancer (PCa) is the most common male reproductive malignancy, with traditional Chinese medicine (TCM) offering potential complementary treatments. Aidi injection, used for liver, lung, and colorectal cancers, shows promise for PCa, but its mechanisms are unclear. This study aims to uncover the molecular pathways through which Aidi injection affects PCa using network pharmacology and experiments.</p><p><strong>Methods: </strong>The study used network pharmacology to identify active components of Aidi injection and their targets from various databases. These targets were cross-referenced with PCa-related targets to uncover therapeutic possibilities. Protein-protein interaction (PPI) and KEGG pathway analyses highlighted key molecular pathways affected by Aidi injection. Molecular docking examined ingredient-target binding. In vitro tests evaluated effects on PCa cell proliferation, apoptosis, and IL-6/STAT3 signaling, while in vivo studies assessed tumor growth and immune response in mice.</p><p><strong>Results: </strong>The study identified 58 active components and 804 PCa-related target genes, with 49 overlapping therapeutic targets. Key compounds such as quercetin, kaempferol, isorhamnetin, and cantharidin were highlighted. Core targets included ESR1, IL-6, STAT3, HSP90AA1, EGFR, and VEGFA. KEGG analysis revealed the IL-6/STAT3 and EGFR pathways as significant in PCa treatment. In vitro, Aidi injection inhibited PCa cell proliferation, induced apoptosis, and suppressed IL-6/STAT3 activation. In vivo, Aidi injection reduced tumor growth and enhanced immune response in mice.</p><p><strong>Conclusions: </strong>Aidi injection influences the IL-6/STAT3 and EGFR pathways, suppressing PCa cell growth, inducing apoptosis, and reducing migration and invasion. These findings offer valuable insights into the therapeutic potential of Aidi injection for prostate cancer.</p>","PeriodicalId":8960,"journal":{"name":"Biological Procedures Online","volume":"27 1","pages":"48"},"PeriodicalIF":4.3,"publicationDate":"2025-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12723836/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145809352","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HCAR2 Orchestrates an Immunosuppressive Niche and Determines Checkpoint Inhibitor Responsiveness in Esophageal Squamous Cell Carcinoma.","authors":"Zekun Li, Guangcong Shen, Xiaoqing Ma, Chenyang Meng, Diliyaer Abudukeremu, Rui Zhao, Zuoyu Chen, Qiang Song, Xiaofan Guo, Tianxing Zhou, Chao Xu, Bo Ni, Yueying Shan, Boyang Fu, Yiheng Chen, Zhansheng Jiang, Yongjie Xie, Kaiyuan Wang, Liangliang Wu, Xiuchao Wang","doi":"10.1186/s12575-025-00305-1","DOIUrl":"10.1186/s12575-025-00305-1","url":null,"abstract":"<p><p>BACKGROUND: Esophageal squamous cell carcinoma (ESCC) is a highly aggressive malignancy with poor prognosis, where immune checkpoint inhibitors (ICIs), such as anti-PD-1/PD-L1 antibodies, show limited efficacy with heterogeneous patient responses. The tumor microenvironment (TME) and tumor subclonal heterogeneity significantly influence immune evasion and therapeutic resistance. This study aimed to identify distinct tumor subpopulations in ESCC, characterize their roles in immunosuppression, and determine their association with ICI responsiveness. METHODS: We analyzed single-cell multi-omics data from tumor specimens and peripheral blood mononuclear cells (PBMCs) of 12 ESCC patients receiving neoadjuvant therapy. Using bioinformatics tools (Seurat, CellChat), we identified tumor subpopulations, inferred cell-cell communication, and validated functional mechanisms via in vitro assays (cell culture, flow cytometry, western blotting), patient-derived organoid (PDO) co-culture systems, and humanized mouse models. Clinical correlations were assessed using bulk transcriptome data, survival analysis, and multi-cohort validation (GEO datasets, IMvigor210 cohort). RESULTS: A distinct HCAR2+ epithelial subclone was identified, characterized by high PD-L1 expression, immunosuppressive cell interactions (e.g., PD-L1/PD-1 axis with exhausted NK-like T cells), and enrichment in pathways driving immune evasion (STAT3, IL-6, PI3K-AKT-mTOR). HCAR2+ cells upregulated PD-L1 via STAT3 activation, impairing CD8+ T cell cytotoxicity and antigen presentation. Clinically, HCAR2+ infiltration correlated with poor prognosis, increased copy number variations (CNVs), high tumor mutational burden (TMB), and enhanced sensitivity to neoadjuvant anti-PD-1 therapy in vivo. Multi-cohort analysis confirmed HCAR2 expression as a predictive biomarker for favorable ICI response, associated with reduced immune exclusion and TIDE scores. CONCLUSIONS: HCAR2+ tumor subclones orchestrate an immunosuppressive TME via PD-L1-mediated CD8+ T cell exhaustion while paradoxically conferring sensitivity to PD-L1 blockade. HCAR2 expression serves as a dual biomarker for poor prognosis and ICI responsiveness, offering a novel molecular target for stratifying ESCC patients who may benefit from neoadjuvant immune checkpoint therapy. Targeting the HCAR2-STAT3-PD-L1 axis could enhance immunotherapy efficacy in this aggressive cancer. </p>","PeriodicalId":8960,"journal":{"name":"Biological Procedures Online","volume":" ","pages":"4"},"PeriodicalIF":4.9,"publicationDate":"2025-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12831423/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145792828","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Arsenic Sulfide Induces Apoptosis in Myelodysplastic Neoplasm Cells Through the Suppression of ABI2.","authors":"Yuchen Tao, Ning Ding, Runfeng Ni, Shuyang Cai, Rui Jin, Yirong Chen, Jianye Ren, Hao Xu, Qian Ba, Jiahui Lu","doi":"10.1186/s12575-025-00311-3","DOIUrl":"10.1186/s12575-025-00311-3","url":null,"abstract":"<p><strong>Background: </strong>Myelodysplastic neoplasms (MDS) are a category of myeloid malignancies that can progress to acute myeloid leukemia (AML). Arsenic sulfide (As₂S₂) has demonstrated efficacy in the treatment of MDS. However, further investigation is required to elucidate its specific therapeutic targets.</p><p><strong>Objective: </strong>To examine the influence of ABI2 on MDS and clarify the regulatory role of As₂S₂ on ABI2 within the therapeutic framework of MDS.</p><p><strong>Methods: </strong>To explore ABI2's role in the expression and prognosis of patients with hematological malignancies, RNA interference was used to reduce ABI2 expression in SKM-1, K562 and MDS-L cell lines. The therapeutic efficacy of As₂S₂ and its regulatory impact on ABI2 were evaluated both in vitro and in vivo.</p><p><strong>Results: </strong>ABI2 was found to be overexpressed in the peripheral blood of patients with MDS and AML, which was significantly associated with decreased survival rates in AML patients. Inhibition of ABI2 decreased the proliferation and increased the apoptosis of SKM-1, K562 and MDS-L cells. As₂S₂ also inhibited cell proliferation and induced apoptosis in these cells, but its efficacy diminished significantly with ABI2 silencing. Additionally, As₂S₂ showed therapeutic benefits in NHD13 mice by downregulating bone marrow ABI2 expression.</p><p><strong>Conclusion: </strong>The collective findings suggest that ABI2 is significantly overexpressed in MDS and AML, and its expression was correlated with unfavorable prognostic outcomes. Furthermore, As₂S₂ demonstrates therapeutic efficacy in MDS by modulating the expression levels of ABI2.</p>","PeriodicalId":8960,"journal":{"name":"Biological Procedures Online","volume":"27 1","pages":"47"},"PeriodicalIF":4.3,"publicationDate":"2025-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12690970/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145712910","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Listening to the Past, Shaping the Future: A Data-mining Based and Visual Analysis of Five Decades of Gastric Carcinogenesis Research.","authors":"Tai Zhang, Xudong Tang","doi":"10.1186/s12575-025-00316-y","DOIUrl":"10.1186/s12575-025-00316-y","url":null,"abstract":"<p><strong>Background: </strong>Gastric cancer remains a major global health concern with approximately one million new cases annually. Despite five decades of extensive research, comprehensive analysis mapping gastric carcinogenesis research evolution and emerging therapeutic frontiers remains limited. This study aims to systematically analyze the intellectual landscape, research trends, and future directions in gastric carcinogenesis research.</p><p><strong>Materials and methods: </strong>We analyzed 11,527 scientific publications on gastric carcinogenesis from 1970-2024 using advanced scientometric tools including CiteSpace and VOSviewer for co-citation analysis, collaboration network mapping, and keyword co-occurrence analysis.</p><p><strong>Results: </strong>Publication output demonstrated exponential growth, peaking at 547 publications in 2022. Asia leads research productivity with China, Japan, and South Korea contributing 37.50% of total publications, while the United States exhibits highest collaborative influence with betweenness centrality of 0.45. Seven distinct research clusters emerged encompassing Helicobacter pylori pathogenesis, molecular mechanisms, precancerous lesions, autoimmune gastritis, and therapeutic interventions. Five emerging trends were identified: stromal microenvironment interactions in carcinogenesis progression, gastric organoid models for disease modeling, artificial intelligence-enhanced endoscopic detection technologies, biomarker development for early diagnosis, and traditional herbal medicine applications for chemoprevention.</p><p><strong>Conclusions: </strong>Research gaps persist in autoimmune gastritis pathways and clinical translation of molecular discoveries. Emerging research directions encompass advanced modeling systems, molecular diagnostics, and technological applications, though their clinical impact remains to be established through future validation studies.</p>","PeriodicalId":8960,"journal":{"name":"Biological Procedures Online","volume":" ","pages":"3"},"PeriodicalIF":4.3,"publicationDate":"2025-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12817797/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145707337","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"(-)-Guaiol Downregulates M2 Tumor-Associated Macrophage Polarization Through PPAR-γ Signaling to Suppress Lung Cancer.","authors":"Zhen-Yu Zhao, Jian-Chun Wu, Ying-Bin Luo, Yu-Li Wang, Xi Wang, Jian-Hui Tian, Bo Zhang, Yan Li","doi":"10.1186/s12575-025-00312-2","DOIUrl":"10.1186/s12575-025-00312-2","url":null,"abstract":"<p><p>BACKGROUND: M2 macrophages play a pivotal role in promoting the growth and metastasis of lung cancer cells. Inhibiting M2 macrophage polarization represents an effective immunotherapeutic approach against tumors. Although (-)-Guaiol has been shown to exert potent inhibitory effects on M2 macrophage polarization, its underlying molecular mechanism remains unclear. OBJECTIVE: This study aimed to elucidate the effects of (-)-Guaiol on M2 macrophage polarization and to explore the potential molecular mechanisms involved. METHODS: Bone marrow-derived macrophages (BMDMs) from mice were polarized toward the M2 phenotype using IL-4 and M-CSF. Both ex vivo and in vivo experiments were performed to determine whether (-)-Guaiol suppresses M2 macrophage polarization through the PPAR-γ-related signaling pathway. PPAR-γ agonists and inhibitors were applied to confirm the involvement of PPAR-γ in the effects of (-)-Guaiol. A co-culture system of M2 macrophages and Lewis lung carcinoma (LLC) cells was established. Wound healing, Transwell invasion, and plate cloning experiments were performed to determine the effects of (-)-Guaiol on the metastasis and development of lung cancer cells. RESULTS: (-)-Guaiol markedly downregulated the expression of CD206, a characteristic surface marker of M2-polarized macrophages. It also significantly inhibited the proliferation, invasion, and metastatic potential of LLC cells co-cultured with M2 macrophages. Animal experiments revealed that (-)-Guaiol treatment significantly decreased the tumor volume and weight, as well as CD206 expression. Moreover, integrated in vitro and in vivo analyses revealed that (-)-Guaiol inhibited M2 macrophage polarization primarily by suppressing the PPAR-γ signaling pathway. CONCLUSION: These findings demonstrate that (-)-Guaiol inhibits M2 macrophage differentiation via targeted suppression of the PPAR-γ-related signaling pathway, thereby reducing the proliferation, migration, and invasion of lung cancer cells. </p>","PeriodicalId":8960,"journal":{"name":"Biological Procedures Online","volume":" ","pages":"1"},"PeriodicalIF":4.9,"publicationDate":"2025-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12801675/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145686801","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Novel Strategy for Enhancing Lung Cancer Immunotherapy Efficacy: Traditional Chinese Medicine Formula Shuyu Pills Enhances Anti-PD-1 Efficacy Via the \"GM-ERS-Immunity\" Axis.","authors":"Sheng Chen, Jing Wen, Zhengyi Liu, Yuxiang Hu, Chenhong Zhu, Xiao Yang, Zhi Wen, Cai Tan, Yaoyao Li, Anqi Xiao, Shuying You, Tonglin Sun, Hua Liu, Yinhui Sun, Lihuai Wang","doi":"10.1186/s12575-025-00314-0","DOIUrl":"10.1186/s12575-025-00314-0","url":null,"abstract":"<p><p>BACKGROUND: Lung cancer remains a leading cause of cancer-related mortality globally. Although immunotherapy with anti-PD-1 monoclonal antibodies has revolutionized treatment, its efficacy is often limited by acquired resistance and a low response rate. The gut microbiota (GM) and endoplasmic reticulum stress (ERS) have emerged as crucial factors influencing the tumor microenvironment and immune responses. Traditional Chinese Medicine (TCM), such as Shuyu Pills (SYP), is being explored for its potential to enhance immunotherapy. This study aimed to investigate the mechanism by which SYP enhances the efficacy of anti-PD-1 therapy in lung cancer, specifically focusing on the “GM-ERS-Immunity” axis. Aim of the study This study aimed to systematically elucidate how the TCM formula Shuyu Pills (SYP) enhances anti-PD-1 mAb therapy in lung cancer by integrating network pharmacology and in vivo validation. METHODS: We established a lung cancer mouse model and treated the mice with SYP, anti-PD-1 monoclonal antibodies, or a combination of both. Tumor growth was monitored, and immune responses were assessed by flow cytometry. To investigate the underlying mechanism, we performed gut microbiota sequencing (16 S rRNA sequencing) and analyzed key markers associated with endoplasmic reticulum stress (ERS) and immunity. Network pharmacology was employed to identify the active components of SYP and their potential targets. RESULTS: We established a lung cancer mouse model and treated the mice with SYP, anti-PD-1 monoclonal antibodies, or a combination of both. Tumor growth was monitored, and immune responses were assessed by flow cytometry. To investigate the underlying mechanism, we performed gut microbiota sequencing (16 S rRNA sequencing) and analyzed key markers associated with endoplasmic reticulum stress (ERS) and immunity. Network pharmacology was employed to identify the active components of SYP and their potential targets. CONCLUSIONS: This study reveals a novel mechanism by which the traditional Chinese medicine formula, SYP, enhances the therapeutic efficacy of anti-PD-1 in lung cancer. By regulating the gut microbiota and subsequently alleviating endoplasmic reticulum stress, SYP potentiates the host’s anti-tumor immunity. These findings provide a strong theoretical basis for the clinical application of SYP as an adjunctive therapy to overcome resistance and improve the effectiveness of anti-PD-1 immunotherapy. </p>","PeriodicalId":8960,"journal":{"name":"Biological Procedures Online","volume":" ","pages":"49"},"PeriodicalIF":4.9,"publicationDate":"2025-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12729002/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145666855","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical Retrospective Study on the Role of Spleen-Invigorating and Qi-Supporting Therapy in Non-Small Cell Lung Cancer Immunotherapy and Construction of Survival Prediction Model.","authors":"Ziyi Chen, Jiangnan Huang, Chun Shen, Yaoyao Li, Zhi Wen, Yinhui Sun, Hua Liu, Lihuai Wang","doi":"10.1186/s12575-025-00310-4","DOIUrl":"10.1186/s12575-025-00310-4","url":null,"abstract":"<p><strong>Objective: </strong>This study aims to evaluate the clinical efficacy of combining spleen‑nourishing and qi‑tonifying therapy with programmed cell death protein 1 (PD‑1)/programmed death‑ligand 1 (PD‑L1) inhibitors in patients with stage IIIB-IV non‑small cell lung cancer (NSCLC), and to develop a survival prediction model based on progression‑free survival (PFS) and overall survival (OS).</p><p><strong>Methods: </strong>A retrospective cohort of 246 patients with stage IIIB-IV NSCLC receiving immunotherapy at the Tumor Medicine Center of the First Hospital of Hunan University of Chinese Medicine from September 2019 to October 2024 is assembled. Patients are categorized into a traditional Chinese medicine (TCM) group (n = 174) or a control group (n = 72) according to use of TCM decoctions. Baseline clinical and pathological characteristics and treatment data are collected. Cox proportional hazards regression is used to analyze survival‑related factors. Kaplan-Meier curves and log‑rank tests are used to compare survival. Logistic regression is used to identify factors associated with the objective response rate (ORR). Survival prediction models based on PFS and OS are constructed and validated.</p><p><strong>Results: </strong>Median PFS is 5.9 months in the TCM group versus 2.9 months in the control group (P < 0.001), and median OS is 22.3 versus 14.8 months (P < 0.001). On multivariable analysis, TCM intervention, PD‑L1 expression, alkaline phosphatase (ALP), lactate dehydrogenase (LDH), and cytokeratin fragment 21‑1 (CYFRA21‑1) are independent predictors of PFS; TCM intervention, brain metastasis, and carcinoembryonic antigen (CEA) independently influence OS. The 6‑month PFS rate, 1‑year PFS rate, and 1‑year OS rate are significantly higher in the TCM combination group than in controls (P < 0.05). TCM intervention and sex are independent predictors of ORR (P < 0.05). Model validation shows areas under the curve (AUCs) of 0.705 (PFS) and 0.636 (OS) in the prediction-model group, and 0.879 (PFS) and 0.765 (OS) for internal validation.</p><p><strong>Conclusion: </strong>The addition of TCM to PD‑1/PD‑L1 inhibitors prolongs PFS and OS in patients with stage IIIB-IV NSCLC. A survival prediction model based on routine clinical characteristics demonstrates predictive utility, offering a potential tool to inform clinical decision‑making.</p>","PeriodicalId":8960,"journal":{"name":"Biological Procedures Online","volume":" ","pages":"2"},"PeriodicalIF":4.3,"publicationDate":"2025-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12805758/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145660271","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrating of Machine Learning to Characterize Tumor-Infiltrating Immune Cell-Related Signature for Enhancing Prognosis for Glioma Patients.","authors":"Chen Yang, JieFei Ma, RanZe Cai, Hong Gao, Fan Hu, QiuPing Li","doi":"10.1186/s12575-025-00308-y","DOIUrl":"10.1186/s12575-025-00308-y","url":null,"abstract":"<p><p>BACKGROUDS: Immunoblockade therapy based on PD-1 checkpoint has shown remarkable progress in various tumors, but its effectiveness in glioma patients is still lacking. Thus, it is in urgent need to uncover an ideal signature for glioma. METHODS: Five cohorts comprised 1973 patients from The Cancer Genome Atlas Program (TCGA), Chinese Glioma Genome Atlas (CGGA), and the Gene Expression Omnibus (GEO) database were included in the present study. By performing consensus clustering, limma and survival analysis, 42 prognostic genes were screened. Subsequently, a consensus immune cell infiltration-related signature (IRS) was developed using a 10-fold cross-validation framework with 101 combinations of 10 machine-learning algorithms, and the predictive performance of IRS was comprehensively analyzed. Ultimately, we evaluated the response of distinct risk subgroups to screen candidate drugs designed to address specific risk factors in the backgrounds of personalized medicine. RESULTS: Three molecular subtypes with distinct immune status and survival outcome were identified through consensus clustering analysis. By performing machine learning analysis on the common differentially expressed genes (DEGs), a consensus IRS was developed by the combined StepCox[both] + SuperPC algorithm. The IRS demonstrated high accuracy and robustness performance across multiple cohorts including TCGA, CGGA-693, CGGA325, GSE16011 and GSE43378. Moreover, the IRS could independently predict the survival outcome regardless of the impact of other clinical variables. Compared to the low IRS group, patients in the high IRS group are more sensitive to the chemotherapy drugs, while low IRS group patients may receive benefits from immunotherapy. Additionally, several candidate drugs were screened from multiple databases for poor survival outcome patients. Notably, a novel biomarker, C1QB, from the IRS, was highly expressed in glioma tissue and promotes progression in U87 cells by enhancing proliferative and migratory capacities while inhibiting apoptosis. CONCLUSIONS: The IRS could accurately predict glioma patients survival and may contribute to the development of personalized therapy. Moreover, as a key gene in IRS, over expression of C1QB could significantly enhance glioma cell viability. </p>","PeriodicalId":8960,"journal":{"name":"Biological Procedures Online","volume":"27 1","pages":"46"},"PeriodicalIF":4.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12667129/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145653556","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}