Cancer Biology & Therapy最新文献_第2页

A comparison of cell death pathways in three different kinds of human lung cancer cell lines following hematoporphyrin derivative-mediated photodynamic therapy. 血卟啉衍生物介导的光动力治疗后三种不同类型人肺癌细胞系细胞死亡途径的比较

IF 4.6 4区医学

Cancer Biology & Therapy Pub Date : 2025-12-01 Epub Date: 2025-08-02 DOI: 10.1080/15384047.2025.2542011

Yijiang Ma, Baohong Xiao, Aihua Sui, Xiaohui Yang, Shichao Cui, Yiwei Cao, Cunzhi Lin

{"title":"A comparison of cell death pathways in three different kinds of human lung cancer cell lines following hematoporphyrin derivative-mediated photodynamic therapy.","authors":"Yijiang Ma, Baohong Xiao, Aihua Sui, Xiaohui Yang, Shichao Cui, Yiwei Cao, Cunzhi Lin","doi":"10.1080/15384047.2025.2542011","DOIUrl":"10.1080/15384047.2025.2542011","url":null,"abstract":"This study was conducted to investigate the in vitro differences in killing effects and cellular death pathways in human bronchial epithelial BEAS-2B cells, human lung adenocarcinoma A549 cells, human lung squamous carcinoma H520 cells, and human lung small cell carcinoma H446 cells mediated by hematoporphyrin derivative (HPD) at 630 nm laser wavelength. Our results showed that the viability of the BEAS-2B, A549, H520, and H446 cells gradually decreased with increasing HPD concentration after HPD-PDT. HPD-PDT induced an increase in intracellular ROS production (p < 0.05), with H520 > A549 > H446 > BEAS-2B. HPD-PDT resulted in intracellular chromatin fixation and dense nuclear staining and induced apoptosis, with apoptosis rates of H520 > A549 > H446 > BEAS-2B. The western blotting (WB) results showed that HPD-PDT could lead to reduced BCL-2 protein levels, upregulate BAX protein expression and activate caspase-3 protein, and induce autophagy, as evidenced by the increased expression of the autophagy-related proteins ATG5, Beclin-1 and LC3B in all cells tested. However, apoptosis-inducing proteins and autophagy proteins were statistically different in these four cell types. Our study confirms that HPD-mediated phototoxicity varied in the different cell lines, indicating that lung cancer cells die due to the interactions of different cell death pathways rather than the same well-defined mechanisms.","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2542011"},"PeriodicalIF":4.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12320871/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144768390","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}

引用次数: 0

Unraveling the dual role of METTL3-mediated m⁶A RNA modification in bladder cancer: mechanisms, therapeutic vulnerabilities, and clinical implications. 揭示mettl3介导的m6A RNA修饰在膀胱癌中的双重作用：机制、治疗脆弱性和临床意义。

IF 4.6 4区医学

Cancer Biology & Therapy Pub Date : 2025-12-01 Epub Date: 2025-08-08 DOI: 10.1080/15384047.2025.2545057

Hua Chun, Kangzhuo Baima

引用次数: 0

Definitive chemoradiotherapy combined with anti-PD-1 immunotherapy for inoperable esophageal squamous cell carcinoma: a multicenter real-world study. 明确放化疗联合抗pd -1免疫疗法治疗不能手术的食管鳞状细胞癌：一项多中心现实世界研究

IF 4.4 4区医学

Cancer Biology & Therapy Pub Date : 2025-12-01 Epub Date: 2025-05-14 DOI: 10.1080/15384047.2025.2504726

Xiongtao Yang, Xiaomin Wang, Qin Xiao, Xiaolin Ge, Nuo Yu, Jiao Li, Guojie Feng, Ziyu Zheng, Yingying Jiang, Lin Lu, Xiaojie Xia, Lei Deng, Tao Zhang, Wenqing Wang, Wenyang Liu, Jianyang Wang, Zefen Xiao, Zongmei Zhou, Nan Bi, Hui Wang, Cheng Chen, Xin Wang

引用次数: 0

Adipose-Derived Exosomes: mediators of crosstalk between Adipose tissue and cancer. 脂肪衍生外泌体：脂肪组织与癌症之间的串扰介质。

IF 4.6 4区医学

Cancer Biology & Therapy Pub Date : 2025-12-01 Epub Date: 2025-08-16 DOI: 10.1080/15384047.2025.2547564

Changjian Wang, Zhikun Zheng, Chuangyan Wu, Dan Zhang, Yangchenxi Wang, Sheng Zhang, Geng Wang, Rui Zhou

{"title":"Adipose-Derived Exosomes: mediators of crosstalk between Adipose tissue and cancer.","authors":"Changjian Wang, Zhikun Zheng, Chuangyan Wu, Dan Zhang, Yangchenxi Wang, Sheng Zhang, Geng Wang, Rui Zhou","doi":"10.1080/15384047.2025.2547564","DOIUrl":"10.1080/15384047.2025.2547564","url":null,"abstract":"Adipose-derived exosomes (ADEs), a subtype of extracellular vesicles, are critical mediators of communication between adipose tissue and tumors, playing pivotal roles in cancer progression and therapeutic response. These nanoscale vesicles carry microRNAs, proteins, and lipids that influence tumor cell proliferation, migration, metastasis, and immune modulation. The dual functions of ADEs - both in promoting and suppressing tumorigenesis - are largely dependent on their cellular origin, molecular cargo, and the characteristics of the tumor microenvironment. Recent studies have identified ADEs as potential diagnostic biomarkers, therapeutic targets, and drug delivery platforms, offering promising avenues for precision oncology. However, significant challenges - such as biological heterogeneity, lack of standardization in production, concerns regarding efficacy and safety, and regulatory constraints - continue to hinder their clinical translation. This review aimed to explore the multifaceted roles of ADEs in cancer pathogenesis, their therapeutic potential, and current limitations, providing insights to guide future research and clinical applications.","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2547564"},"PeriodicalIF":4.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12360202/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144858871","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}

引用次数: 0

Lenvatinib promotes hepatocellular carcinoma pyroptosis by regulating GSDME palmitoylation. Lenvatinib通过调节GSDME棕榈酰化促进肝癌细胞焦亡。

IF 4.4 4区医学

Cancer Biology & Therapy Pub Date : 2025-12-01 Epub Date: 2025-07-13 DOI: 10.1080/15384047.2025.2532217

Yuan Yuan, Mu-Ru Wang, Yang Ding, Ya Lin, Ting-Ting Xu, Xing-Xing He, Pei-Yuan Li

{"title":"Lenvatinib promotes hepatocellular carcinoma pyroptosis by regulating GSDME palmitoylation.","authors":"Yuan Yuan, Mu-Ru Wang, Yang Ding, Ya Lin, Ting-Ting Xu, Xing-Xing He, Pei-Yuan Li","doi":"10.1080/15384047.2025.2532217","DOIUrl":"10.1080/15384047.2025.2532217","url":null,"abstract":"Lenvatinib, as a multi-kinase inhibitor, has been approved as a first-line drug for patients with advanced hepatocellular carcinoma (HCC). Gasdermin E (GSDME)-mediated pyroptosis, a form of programmed cell death, can be induced by chemotherapy drugs or certain kinase inhibitors. However, the role of Lenvatinib in inducing pyroptosis in HCC warrants further investigation. Phase contrast microscopy, LDH assays, and gain- and loss-of-function strategies were used to evaluate Lenvatinib-induced pyroptosis in HCC cells. GSDME palmitoylation was assessed via the acyl-biotin exchange method. In vivo, a subcutaneous HCC xenograft model in nude mice were established to assess the effects of interfering with GSDME on the sensitivity of HCC to Lenvatinib. Lenvatinib induced pyroptosis in HCC cells in a dose- and time-dependent manner. Additionally, Lenvatinib promoted GSDME cleavage, with upregulation of GSDME enhancing pyroptosis and downregulation reducing this effect. The ABE method revealed that GSDME is palmitoylated, and Lenvatinib increased its palmitoylation, promoting plasma membrane localization and enhancing protein stability. Inhibition of GSDME palmitoylation by 2-BP blocked Lenvatinib-induced pyroptosis. In vivo, upregulation of GSDME increased HCC sensitivity to Lenvatinib and inhibited tumor growth. Lenvatinib induces pyroptosis in HCC by promoting the palmitoylation of GSDME, enhancing its localization to the plasma membrane and increasing its protein stability. Interfering with GSDME, both in vitro and in vivo, affects Lenvatinib-induced pyroptosis, thereby altering the therapeutic sensitivity of HCC to Lenvatinib. Targeting GSDME palmitoylation represents a potential therapeutic strategy for HCC, as it enhances Lenvatinib-induced pyroptosis and improves the therapeutic response.","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2532217"},"PeriodicalIF":4.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12269688/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144625328","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}

引用次数: 0

MGAT4EP promotes tumor progression and serves as a prognostic marker for breast cancer. MGAT4EP 可促进肿瘤进展，是乳腺癌的预后标志物。

IF 4.4 4区医学

Cancer Biology & Therapy Pub Date : 2025-12-01 Epub Date: 2025-03-11 DOI: 10.1080/15384047.2025.2475604

Lin Zhong, Jianfeng Zhu, Jie Chen, Xuchu Jin, Liangquan Liu, Shufeng Ji, Jing Luo, Hong Wang

{"title":"MGAT4EP promotes tumor progression and serves as a prognostic marker for breast cancer.","authors":"Lin Zhong, Jianfeng Zhu, Jie Chen, Xuchu Jin, Liangquan Liu, Shufeng Ji, Jing Luo, Hong Wang","doi":"10.1080/15384047.2025.2475604","DOIUrl":"10.1080/15384047.2025.2475604","url":null,"abstract":"Breast cancer remains a global health challenge with varied prognoses despite treatment advancements. Therefore, this study explores the pseudogene MGAT4EP as a potential biomarker and therapeutic target in breast cancer. Using TCGA data and bioinformatics, MGAT4EP was identified as significantly overexpressed in breast cancer tissues and associated with poor prognosis. Multivariate Cox regression confirmed MGAT4EP as important prognostic factor. A clinical prediction model based on MGAT4EP expression showed high accuracy for 1-, 3-, and 5-year survival rates and was translated into a nomogram for clinical application. Functional studies revealed that silencing MGAT4EP via siRNA promoted apoptosis, inhibited migration and invasion in breast cancer cells. RNA-seq, GSEA, and GO analyses linked MGAT4EP to apoptosis and focal adhesion pathways. Notably, knock down of MGAT4EP significantly suppressed tumor growth and metastasis in xenograft and lung metastasis models. Taken together, these findings establish MGAT4EP as an attractive target for metastatic breast cancer and provide a potential a promising therapeutic target for breast cancer treatment.","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2475604"},"PeriodicalIF":4.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11901376/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143603991","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}

引用次数: 0

Effect of extracellular vesicle ZNF280B derived from lung cancer stem cells on lung cancer progression. 肺癌干细胞来源的细胞外囊泡ZNF280B对肺癌进展的影响

IF 4.4 4区医学

Cancer Biology & Therapy Pub Date : 2025-12-01 Epub Date: 2025-01-17 DOI: 10.1080/15384047.2025.2450849

Qixia Guo, Jiayan Lu, Hui Zhao, Ding Zhou, Hua Liu

{"title":"Effect of extracellular vesicle ZNF280B derived from lung cancer stem cells on lung cancer progression.","authors":"Qixia Guo, Jiayan Lu, Hui Zhao, Ding Zhou, Hua Liu","doi":"10.1080/15384047.2025.2450849","DOIUrl":"10.1080/15384047.2025.2450849","url":null,"abstract":"Objective: The purpose of this research was to investigate the role of extracellular vesicles derived from lung cancer stem cells (lung CSCs-EVs) in lung cancer and to explore their potential mechanisms.Methods: Lung CSCs were first isolated and verified using flow cytometry and RT-qPCR assays. Lung CSCs-EVs were extracted through ultracentrifugation and further characterized using transmission electron microscopy and Western blotting. The interaction between lung CSCs-EVs and lung cancer cells was observed through PKH67 staining. Subsequently, we analyzed the differentially expressed genes in lung CSCs using bioinformatics data analysis and evaluated the prognostic value of ZNF280B in lung cancer with the Kaplan-Meier Plotter. RT-qPCR was utilized to assess the mRNA expression levels of these genes, while Western blotting was used to evaluate the protein expression levels of ZNF280B and P53. Next, CCK-8 and colony formation assays were conducted to assess the effects of lung CSCs-EVs and ZNF280B on cancer cell proliferation, migration (via wound healing assay), and invasion (using transwell assay). Additionally, subcutaneous tumor-bearing experiments in nude mice were performed to evaluate the roles of lung CSCs-EVs in lung cancer progression in vivo.Results: The results indicated that lung CSCs-EVs accelerated the progression of lung cancer. Mechanistically, these lung CSCs-EVs transferred ZNF280B into cancer cells, leading to the inhibition of P53 expression.Conclusions: In summary, the manuscript first describes the molecular mechanism by which lung CSCs-EVs promote pro-cancer functions in lung cancer through the ZNF280B/P53 axis.","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2450849"},"PeriodicalIF":4.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143000794","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Assessing the potential for in vivo modulation of FTH1 gene expression with small peptides to restore and enhance androgen receptor pathway inhibition in prostate cancer. 评估小肽在体内调节FTH1基因表达以恢复和增强前列腺癌雄激素受体通路抑制的潜力。

IF 4.4 4区医学

Cancer Biology & Therapy Pub Date : 2025-12-01 Epub Date: 2025-05-09 DOI: 10.1080/15384047.2025.2503417

Crawford Currie, Christian Bjerknes, McKayla Nicol, Sateesh Kumar, Bomi Framroze

{"title":"Assessing the potential for in vivo modulation of FTH1 gene expression with small peptides to restore and enhance androgen receptor pathway inhibition in prostate cancer.","authors":"Crawford Currie, Christian Bjerknes, McKayla Nicol, Sateesh Kumar, Bomi Framroze","doi":"10.1080/15384047.2025.2503417","DOIUrl":"https://doi.org/10.1080/15384047.2025.2503417","url":null,"abstract":"Increased levels of intratumoral free iron drive more aggressive behavior with the development of treatment resistance and spread in a range of cancers including prostate cancer (PCa). This phenotype is associated with an increase in TFRC expression and a decrease in FTH1, a profile supporting increased iron acquisition. In this study we investigated the anti-oncogenic effects of two small peptides (FT-002 and FT-005) that upregulate FTH1 expression and downregulate TFRC expression when combined with standard androgen receptor pathway inhibitors (ARPIs) in xenograft models of PCa in male athymic nude mice. The PC3 cell line was used to establish xenografts representing highly aggressive, androgen-resistant PCa and the LNCaP cell line as a model of androgen-sensitive PCa. Both peptides enhanced the anti-tumor efficacy of ARPI therapy. Efficacy was more marked with the combination of the second-generation APRI enzalutamide than the first-generation agent bicalutamide, a result consistent with known resistance mechanisms to different ARPI therapy. Further, the FT-peptide/enzalutamide combination drove tumor regression whereas enzalutamide monotherapy only slowed growth, even in the hormone-sensitive xenograft. The FT-002a-enzalutamide combination was more effective than FT-005 in reducing tumor mass and volume and modulating FTH1 and TFRC expression. The reversal by the peptides of this oncogenic expression pattern points to a reduction in the tumor free iron via increased iron storage in ferritin and a reduction in iron influx via the transferrin receptor. Peptide-mediated modulation of tumor iron metabolism may therefore offer a novel means to enhance ARPI efficacy and delay resistance in advanced prostate cancer.","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2503417"},"PeriodicalIF":4.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12068333/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143954609","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}

引用次数: 0

Exosomal miR-122-5p for regulation of secretory functions of fibroblasts and promotion of breast cancer metastasis by targeting MKP-2: an experimental study. 外泌体miR-122-5p通过靶向MKP-2调控成纤维细胞分泌功能并促进乳腺癌转移的实验研究

IF 4.4 4区医学

Cancer Biology & Therapy Pub Date : 2025-12-01 Epub Date: 2025-05-04 DOI: 10.1080/15384047.2025.2500104

Yun Lv, Yue Li, Jie Zhou, Xin Liu, Dandan Wang, Dongmei Wang, Dandan Tong, Shuhuai Wang, Hanxiang An, Xinmei Kang

{"title":"Exosomal miR-122-5p for regulation of secretory functions of fibroblasts and promotion of breast cancer metastasis by targeting MKP-2: an experimental study.","authors":"Yun Lv, Yue Li, Jie Zhou, Xin Liu, Dandan Wang, Dongmei Wang, Dandan Tong, Shuhuai Wang, Hanxiang An, Xinmei Kang","doi":"10.1080/15384047.2025.2500104","DOIUrl":"https://doi.org/10.1080/15384047.2025.2500104","url":null,"abstract":"Tumor metastasis is a major obstacle for the effective treatment of breast cancer. Some studies showed that exosomes could promote tumor distant metastasis by establishing pre-metastasis niches (PMN). MicroRNAs (miRNAs) in exosomes play a critical role in tumor development and invasion. We aimed to investigate the effects of exosomal miRNAs derived from breast cancer cells on metastasis. MiRNA sequencing and RT-PCR approach were used to screen potential exosomal miRNAs. We compared the levels of serum exosomal miRNAs from breast cancer patients and those from MCF10A/MCF7/MDA-MB-231 cells. We found that differential exosomal miRNAs screened from patients with metastasis have higher expression levels in exosomes secreted by MDA-MB-231 cells. Using miRNA mimics or inhibitors, exosomal miR-122-5p was found to enhance the secretion levels of chemokine MCP-1 and SDF-1 from WI-38 lung fibroblast cells. In vitro luciferase assay and western blot confirmed the targeting of 3'-untranslated region of MKP-2 and suppression of MKP-2 expression by miR-122-5p in WI-38 cells. Treatment of xenograft mice with exosomal miR-122-5p increased the levels of MCP-1 and SDF-1 in serum, and promoted lung metastasis of breast cancer. In conclusion, we identified exosomal miR-122-5p from breast cancer cells that could promote the chemokine secretion of lung fibroblasts, which might facilitate the chemotaxis and colonization of breast cancer cells in lung tissue.","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2500104"},"PeriodicalIF":4.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12051585/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143968732","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}

引用次数: 0

Correction. 修正。

IF 4.4 4区医学

Cancer Biology & Therapy Pub Date : 2025-12-01 Epub Date: 2025-06-14 DOI: 10.1080/15384047.2025.2520651

引用次数: 0