{"title":"Expression characteristics and biological significance of exosome-related genes in lung cancer.","authors":"Qixiang Zhong, Yujie Zhao","doi":"10.1007/s12672-025-03173-z","DOIUrl":"10.1007/s12672-025-03173-z","url":null,"abstract":"<p><strong>Background: </strong>Lung cancer stands as one of the most prevalent malignancies globally, with its high morbidity and mortality intimately associated with its inconspicuous early symptoms, the advanced stages at diagnosis, and resistance to conventional therapeutic interventions. Exosomes, serving as pivotal mediators of intercellular communication, carry biomolecules that play crucial roles in tumorigenesis, progression, and metastasis, holding promise as novel targets for early diagnosis, prognostic evaluation, and treatment of lung cancer.</p><p><strong>Methods: </strong>In this study, lung cancer-related datasets were obtained from the GEO database and TCGA. Through differential gene analysis, enrichment analysis, immune infiltration analysis, and drug regulatory analysis, exosome-associated genes pertinent to lung cancer were screened and identified.</p><p><strong>Results: </strong>The research revealed significant downregulation of CRYAB, CAV1, HYAL1, and TUBB6 genes in lung cancer tissues, whereas SERINC2, PAICS, SLC2A1, and BIRC5 genes were markedly upregulated. These genes were predominantly enriched in biological processes such as cell migration, oxidative stress response, and cell cycle regulation, as well as in KEGG pathways like the IL-17 signaling pathway. Immune infiltration analysis demonstrated a high correlation between these genes and the infiltration levels of various immune cells. Furthermore, through drug-gene enrichment analysis and molecular docking experiments, significant correlations were found between drugs such as celecoxib and some exosome-related genes, with interaction targets existing between these drugs and CAV1, SLC2A1, and BIRC5 genes.</p><p><strong>Conclusion: </strong>This study unveils the expression characteristics and biological significance of exosome-associated genes in lung cancer. The differential expression of these genes not only offers potential biomarkers for early diagnosis of lung cancer but also lays a foundation for further research into their biological functions in this disease.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"1373"},"PeriodicalIF":2.8,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12274178/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144667404","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Recent advances on the role of G0S2.","authors":"Xin Hua Zhao, Liqin Ruan","doi":"10.1007/s12672-025-03198-4","DOIUrl":"10.1007/s12672-025-03198-4","url":null,"abstract":"<p><p>G0S2, formally known as G0/G1 switch gene 2, functions as an inhibitor of adipose triglyceride lipase (ATGL), a key enzyme in lipolysis that hydrolyzes triglycerides (TG) to diacylglycerol and fatty acid (FA). G0S2 can directly interact with ATGL, suppressing its hydrolase activity. Recently, G0S2 has been implicated in immune system abnormalities, chronic inflammation, and tumorigenesis. However, the underlying mechanisms and roles of G0S2 in immune system disorders and cancer remain incompletely understood. In this review, we provide an overview of the current knowledge on G0S2, highlighting its regulation at different levels and unveiling its potential as a diagnostic and prognostic marker in immune-related diseases and cancer. The discussion covers the roles of G0S2 in lipolysis, lipid synthesis, inflammation, and various cancers.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"1362"},"PeriodicalIF":2.8,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12274192/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144658684","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Vivek Kumar Morya, Anuja Gajanan Magar, Sin-Hye Park, Kyu-Cheol Noh
{"title":"Systemic strategies for osteosarcoma: advances and future directions.","authors":"Vivek Kumar Morya, Anuja Gajanan Magar, Sin-Hye Park, Kyu-Cheol Noh","doi":"10.1007/s12672-025-02208-9","DOIUrl":"10.1007/s12672-025-02208-9","url":null,"abstract":"<p><p>Osteosarcoma is a common and aggressive bone cancer in children and adolescents, typically affecting the long bones during growth spurts. Treatment involves a combination of surgery, chemotherapy, and radiotherapy. Although surgery has become more limb-preserving, the overall prognosis remains challenging, with a 5-year survival rate of 60-70% for localized disease and much lower for advanced stages. Chemotherapy is the mainstay treatment; however, it can cause severe side effects. Targeted therapies (e.g., IGF-1R inhibitors, TKIs) and immunotherapy (e.g., checkpoint inhibitors, CAR-T therapies) are promising areas of research that aim to attack cancer cells more precisely with lower toxicity. Other novel approaches, such as gene therapy and drug delivery systems, are being explored. With continued research and development of new therapies, we hope to significantly improve the outlook of patients with osteosarcoma in the future.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"1367"},"PeriodicalIF":2.8,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12274193/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144658685","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Non-coding RNAs and Hippo signaling in non-small cell lung cancer: emerging roles as biomarkers and therapeutic targets.","authors":"Mohammadamin Joulani, Nahal Aghajamal, Masoumeh Nouri, Faraz Rahmani Khajeh, Nafiseh Sharifi, Dena Saghafi, Mahan Amiri, Ali Abdollahzadeh, Ehsan Heidari, Amin Mirdamadian, Malihe Sharafi, Samira Masoumi, Reza Morovatshoar, Alireza Azani, Qumars Behfar","doi":"10.1007/s12672-025-03099-6","DOIUrl":"10.1007/s12672-025-03099-6","url":null,"abstract":"<p><p>The most common type of cancer and one with a high death rate is lung cancer, especially non-small cell lung cancer (NSCLC), which is mostly brought on by medication resistance, metastasis, and delayed diagnosis. The discovery of non-coding RNAs (ncRNAs), such as circular RNAs (circRNAs), long non-coding RNAs (lncRNAs), and microRNAs (miRNAs), has revealed their vital involvement in the pathophysiology of lung cancer by controlling important cellular processes. The Hippo signaling pathway is one of the critical routes impacted by non-coding RNAs. It is involved in tumor suppression, apoptosis, and cell proliferation. The interaction between ncRNAs and the Hippo pathway in lung cancer is reviewed in this review, with an emphasis on the potential of these molecules as therapeutic targets as well as diagnostic and prognostic biomarkers.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"1365"},"PeriodicalIF":2.8,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12274179/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144658680","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Regulation of GLI2 by LINC02560 and its role in hepatocellular carcinoma.","authors":"Yunmei Huang, Zhang Qingyun, Chunying Luo","doi":"10.1007/s12672-025-03162-2","DOIUrl":"10.1007/s12672-025-03162-2","url":null,"abstract":"<p><p>This article focuses on the regulation of GLI2 by LINC02560 in HCC. Revealing this mechanism provides a new perspective for the morbidity mechanism and treatment strategy of hepatocellular carcinoma.LINC02560, a long non-coding RNA (lncRNA), is upregulated in hepatocellular carcinoma through interaction with GLI2 protein. They jointly regulate key biological processes such as cell proliferation, invasion, migration and apoptosis. It was found that LINC02560 not only directly binds to GLI2 protein, It also plays a regulatory role by affecting the epigenetic modification of GLI2 gene and the interaction with other transcription factors. These mechanisms contribute to the initiation and progression of HCC. In addition, the expression level of LINC02560 is closely related to the therapeutic effect and prognosis of hepatocellular carcinoma. It provides an important basis for the formulation of individualized treatment plan. Therefore, the study of GLI2 regulation by LINC02560 not only deepens our understanding of the mechanism of morbidity in hepatocellular carcinoma, It also provides important clues for finding new therapeutic targets and improving therapeutic effects.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"1372"},"PeriodicalIF":2.8,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12274155/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144667408","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"A case report of adenoid cystic carcinoma combined with giant renal metastasis treated with robotic surgery.","authors":"Yongrui Zhang, Shuxin Li, Yueqiu Zhang, Fulin Wang, Tong Yang, Wei Wei","doi":"10.1007/s12672-025-03197-5","DOIUrl":"10.1007/s12672-025-03197-5","url":null,"abstract":"<p><p>Adenoid cystic carcinoma (ACC) is a rare head and neck tumor with low incidence, characterized by local recurrence and early metastasis following surgical treatment. The common sites of metastasis for this cancer are typically the lungs, liver, brain, and bone, while metastasis to the kidneys is rare. This article reports a case of renal metastasis in a patient with adenoid cystic carcinoma of the maxillary sinus, occurring 16 years after surgery. The patient was a 34-year-old female with intermittent right lower abdominal pain for five months. She was diagnosed with maxillary sinus ACC 16 years ago and was treated surgically with adjuvant radiotherapy three times without regular follow-up. The patient underwent a robotic-assisted unilateral nephrectomy, and pathological examination confirmed the diagnosis of renal metastasis from adenoid cystic carcinoma. Postoperatively, the patient's abdominal pain resolved, and she was discharged on the fifth day with instructions for regular follow-up. During her first follow-up nine months later, she reported no discomfort and confirmed a smooth recovery. This case highlights the potential for late recurrence of adenoid cystic carcinoma, underscoring the importance of long-term follow-up and vigilant monitoring, even after successful initial treatment. Continued surveillance and refinement of treatment strategies are crucial for managing this challenging malignancy.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"1368"},"PeriodicalIF":2.8,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12274180/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144658614","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yanlin Jiang, Yi Fu, Xinyan Song, Yongjie Xie, Xiaobin Shang, Xi Liang
{"title":"The role of UBR2 in triple-negative breast cancer and its implications for immune checkpoint blockade therapy.","authors":"Yanlin Jiang, Yi Fu, Xinyan Song, Yongjie Xie, Xiaobin Shang, Xi Liang","doi":"10.1007/s12672-025-03153-3","DOIUrl":"10.1007/s12672-025-03153-3","url":null,"abstract":"<p><strong>Objective: </strong>UBR2 (also referred to as n-recognin 2, the E3 component of ubiquitin protein ligase) targets proteins with unstable N-terminal residues for polyubiquitination and proteasome-mediated degradation. It was initially identified as a crucial oncogene during embryonic development. Nevertheless, the function of UBR2 in triple-negative breast cancer (TNBC) and its non-ubiquitination role, particularly in suppressing antitumor immune responses, remain elusive.</p><p><strong>Methods: </strong>Utilizing bulk RNA and single-cell RNA sequencing datasets from the GEO and TCGA databases, differentially expressed genes (DEGs) were discerned. Moreover, the relationship between UBR2 and PD-L1 was verified via overexpression viruses, shRNA viruses, and Western blotting. In addition, the correlation between UBR2 and immunotherapy was investigated by means of flow cytometry and immune-infiltration analysis in both in vivo and in vitro experiments.</p><p><strong>Results: </strong>In the cohort of TNBC patients presenting an immune desert microenvironment, as well as in the group of patients responding poorly to PD-L1/PD-1 therapy, UBR2 exerted a significant impact on the establishment of an immunosuppressive microenvironment. The inhibition of UBR2 could diminish the expression of PD-L1 in TNBC cell lines. In addition, the expression level of UBR2 could act as a potential indicator for PD-L1 therapy in TNBC patients, where higher UBR2 expression suggests greater responsiveness to PD-L1 therapy. Concurrently, we screened for inhibitors (11-oxo-mogroside V) targeting the functional domain of UBR2, and concurrent inhibition of UBR2 in combination with PD-L1 therapy can reduce the tumor burden in TNBC.</p><p><strong>Conclusion: </strong>Our findings indicate that the inhibition of UBR2 can augment TIL infiltration by diminishing PD-L1 expression, thereby emerging as an efficacious strategy (the functional inhibitors of UBR2) to enhance the therapeutic efficacy of PD-L1/PD1 blockers, offering a novel perspective for the treatment of TNBC through combined immunotherapy.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"1357"},"PeriodicalIF":2.8,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12271019/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144658686","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Integration of single cell and bulk transcriptomes identifies T cell stress subtypes in LUAD.","authors":"Shengping Min, Linfeng Pan, Xinyu Zhang, Huili Chen, Lixuan Qiu, Xinyu Wang, Yiluo Xie, Kai Zhang, Qiang Zhang, Chaoqun Lian, Jing Zhang","doi":"10.1007/s12672-025-03170-2","DOIUrl":"10.1007/s12672-025-03170-2","url":null,"abstract":"<p><strong>Background: </strong>The unique stress response state of T cells (Tstr) is found in various cancers and correlates with altered Lung Adenocarcinoma (LUAD) tumor microenvironment and immunotherapy outcomes. However, fewer studies have been described on the relationship between Tstr and LUAD, and its mechanism of action in the pathogenesis of LUAD needs to be further investigated.</p><p><strong>Methods: </strong>The categorization and validation of cluster types for Tstr signature genes were systematically carried out using transcriptomic data sourced from the TCGA and GEO databases. The focus was on elucidating distinct pharmacological characteristics, tumor microenvironmental traits, and immunotherapeutic benefits across various subtypes. Moreover, a predictive model was developed through Least Absolute Shrinkage and Selection Operator (LASSO) regression analysis, and subsequent cellular experiments confirmed the pivotal role of CREG2 in driving LUAD cell proliferation and migration.</p><p><strong>Results: </strong>Tstr signature genes represented by the heat shock protein family are highly expressed at the end of T-cell differentiation and affect cellular communication. Patients with the C1 subtype have a poorer prognosis and high expression of HSPA1A and HSPA1B, which exhibit cold tumor characteristics and define them as important Tstr subtypes. CREG2 is positioned as a promising biological indicator as it plays an important part in enhancing the migratory and proliferative capacity of LUAD cells.</p><p><strong>Discussion: </strong>This study reveals the characteristics of different Tstr types. A predictive model was built to forecast the prognosis of LUAD patients based on the DEGs of the subtype. The exploration delved into the bio-function of CREG2 in the progression of LUAD.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"1360"},"PeriodicalIF":2.8,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12271563/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144658678","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Therapeutic effect of Chelidonium majus hydro-alcoholic extract alone and in combination with oxaliplatin on ovarian cancer cell line.","authors":"Zahra Hashempour, Mehdi Noraddini, Majid Nejati, Ameneh Jafari, Mahdi Rafiyan, Amirreza Ostadian, Behrang Alani, Hamed Mirzaei","doi":"10.1007/s12672-025-03081-2","DOIUrl":"10.1007/s12672-025-03081-2","url":null,"abstract":"<p><p>Ovarian cancer (OC) is the leading cause of tumor-related deaths among gynecologic cancers. Patients diagnosed with advanced stages of OC urgently require effective therapeutic interventions, but current therapies often fail in patients with recurrent platinum-resistant tumors. Previous research has shown the cytotoxic effects of Chelidonium majus (C. majus) extract on tumors. In this study we have investigated the effects of combined and independent effects of oxaliplatin and C. majus extract on ovarian cancer cell proliferation and apoptosis. Using the OVACR3 cell line as an in vitro model, we applied the MTT assay for cell growth assessment and RT-qPCR to measure caspase-3, β-catenin, and ZEB1 expression. The results demonstrated that both oxaliplatin and C. majus extract significantly inhibited cell growth and promoted apoptosis, with enhanced effects observed when used together. The inhibition of ZEB1 and β-catenin suggest their involvement in the observed anti-cancer effects. Treated groups also showed higher caspase-3 expression compared to controls. Our findings confirm the synergistic potential of combining oxaliplatin and C. majus extract in treating OC, possibly through the ZEB1/β-catenin pathway. Further research is needed to confirm the clinical applicability and underlying mechanisms of this treatment strategy.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"16 1","pages":"1361"},"PeriodicalIF":2.8,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12271002/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144658666","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}