Cancer Biology & Therapy最新文献

Yes-associated protein 1 in cancer: bridging mechanical transduction and epigenetic regulation. 癌症中的yes相关蛋白1：桥接机械转导和表观遗传调控。

IF 4.6 4区医学

Cancer Biology & Therapy Pub Date : 2025-12-31 Epub Date: 2025-09-21 DOI: 10.1080/15384047.2025.2562726

Tingting Liu, Shuo Yu, Lu Zhang, Wenwen Ji, Guangdong Wang, Na Wang, Mengcong Li, Tinghua Hu, Zhihong Shi

引用次数: 0

Patient-derived organoids (PDOs) as a promising platform for personalized treatment of colorectal cancer: current applications and future challenges. 患者源性类器官（PDOs）作为大肠癌个性化治疗的一个有前途的平台：目前的应用和未来的挑战。

IF 4.6 4区医学

Cancer Biology & Therapy Pub Date : 2025-12-31 Epub Date: 2025-10-13 DOI: 10.1080/15384047.2025.2567802

Yan Liu, Yao Zhang, Ran Zhang, Chengzhao Zhang, Xinlu Liu

{"title":"Patient-derived organoids (PDOs) as a promising platform for personalized treatment of colorectal cancer: current applications and future challenges.","authors":"Yan Liu, Yao Zhang, Ran Zhang, Chengzhao Zhang, Xinlu Liu","doi":"10.1080/15384047.2025.2567802","DOIUrl":"10.1080/15384047.2025.2567802","url":null,"abstract":"Colorectal cancer is a heterogeneous and molecularly complex cancer that often leads to poor prognosis. The standard treatment includes surgical resection and adjuvant therapies such as chemotherapy, radiotherapy, targeted therapy, and immunotherapy. However, owing to the individual heterogeneity of patients, the effectiveness of these treatments is difficult to achieve consistently and efficiently. Patient-derived organoids (PDOs), by mimicking key genes, physical, and mechanical cues from the tumor microenvironment, simulates tumor heterogeneity, tissue structure, and molecular characteristics, as well as the cellular interactions within the tumor microenvironment. Additionally, it provides a more physiological and relevant environment for anticancer drug screening and predicting patient responses to personalized approaches, bridging the gap between simplified 2D models and animal models. Here, we review the roles of PDOs in customizing CRC treatment, discussing its roles in predicting drug sensitivity, drug screening, studying drug resistance mechanisms, simulating cell-to-cell interactions, and exploring immunotherapy targets to develop personalized therapies.","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2567802"},"PeriodicalIF":4.6,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12530486/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145285742","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

Unveiling the oncogenic role of lncRNA PIG13-DT in hepatocellular carcinoma progression. 揭示lncRNA PIG13-DT在肝细胞癌进展中的致癌作用

IF 4.6 4区医学

Cancer Biology & Therapy Pub Date : 2025-12-31 Epub Date: 2025-10-09 DOI: 10.1080/15384047.2025.2567797

Hongjie Cai, Song Chen, Shuangyan Tang, Feng Shi, Dan Zeng, Zhiqiang Wu, Fan Wang, Shuqin Huang, Dongbing Li, Wenbo Guo

{"title":"Unveiling the oncogenic role of lncRNA PIG13-DT in hepatocellular carcinoma progression.","authors":"Hongjie Cai, Song Chen, Shuangyan Tang, Feng Shi, Dan Zeng, Zhiqiang Wu, Fan Wang, Shuqin Huang, Dongbing Li, Wenbo Guo","doi":"10.1080/15384047.2025.2567797","DOIUrl":"10.1080/15384047.2025.2567797","url":null,"abstract":"Background: Hepatocellular carcinoma (HCC) is a leading cause of cancer-related mortality due to delayed diagnosis and poor prognosis. Long non-coding RNAs (lncRNAs) are key cancer regulators, yet the role of C1orf21-DT (PIG13-DT) in HCC remains unclear.Methods: We evaluated PIG13-DT expression in HCC and paired adjacent non-tumorous tissues. Functional studies were conducted using cell culture, cell-derived xenotransplantation (CDX) models, and molecular techniques including RNA pull-down, mass spectrometry, RIP-qPCR, and RNA sequencing. We explored the interplay between PIG13-DT, RNA-binding protein YBX3, and USP15 mRNA.Results: PIG13-DT was highly expressed in HCC tissues compared with normal tissues and associated with poor prognosis. Functionally, PIG13-DT enhanced cancer stem cell (CSC) function, reduced reactive oxygen species (ROS) levels, and promoted HCC cell proliferation and migration. Mechanistically, PIG13-DT interacted with YBX3, stabilizing YBX3 and promoting USP15 mRNA translation and stability, thus driving HCC progression. Clinical data from lenvatinib-treated HCC patients showed that PIG13-DT expression was correlated with poor treatment response.Conclusion: Our study identifies a novel PIG13-DT/YBX3/USP15 axis driving HCC progression, suggesting PIG13-DT as a potential biomarker and therapeutic target. This work provides new insights into HCC molecular mechanisms and offers potential diagnostic and therapeutic implications.","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2567797"},"PeriodicalIF":4.6,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12520071/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145249973","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

Loss of ACSL1 fuels ferroptosis resistance in clear cell renal carcinoma. ACSL1缺失促进透明细胞肾癌的铁下垂抵抗。

IF 4.6 4区医学

Cancer Biology & Therapy Pub Date : 2025-12-31 Epub Date: 2025-10-06 DOI: 10.1080/15384047.2025.2567815

Shangguo Wang, Yuxiong Wang, Bin Liu, Dan Zhang, Zehua Zhang, Hongxia Yang, Guangtao Li, Xiaodong Zhao, Jiaxin Liu, Qianhui Li, Yifan Song, Yanghe Zhang, Yishu Wang, Honglan Zhou

{"title":"Loss of ACSL1 fuels ferroptosis resistance in clear cell renal carcinoma.","authors":"Shangguo Wang, Yuxiong Wang, Bin Liu, Dan Zhang, Zehua Zhang, Hongxia Yang, Guangtao Li, Xiaodong Zhao, Jiaxin Liu, Qianhui Li, Yifan Song, Yanghe Zhang, Yishu Wang, Honglan Zhou","doi":"10.1080/15384047.2025.2567815","DOIUrl":"10.1080/15384047.2025.2567815","url":null,"abstract":"Background: Clear cell renal cell carcinoma (ccRCC), the most common kidney cancer subtype, is marked by lipid metabolism reprogramming and therapy resistance. Ferroptosis-an iron-dependent, lipid peroxidation-driven cell death-has gained attention as a therapeutic strategy. This study investigates the role of ACSL1, a key lipid metabolism enzyme, in ccRCC.Methods: Using TCGA/GEO datasets, qPCR, immunohistochemistry, and immunofluorescence, ACSL1 expression and clinical significance were analyzed. Functional assays with ACSL1-overexpressing ccRCC cells and a xenograft mouse model evaluated its impact on tumor behavior. Transcriptomics and lipidomics, alongside ROS, ferroptosis, and p53 inhibitors, were applied to uncover mechanisms.Results: ACSL1 is markedly downregulated in ccRCC and predicts poor prognosis. Overexpression suppressed proliferation and migration, induced cell death, and slowed tumor growth. Mechanistically, ACSL1 elevated ROS, activated p53, downregulated SLC7A11/GPX4, and triggered ferroptosis. Blocking ROS or p53 reversed these effects, confirming a ROS-p53-SLC7A11/GPX4 feedback loop.Conclusion: ACSL1 functions as a tumor suppressor in ccRCC by inducing ferroptosis via the ROS-p53-SLC7A11/GPX4 axis. It holds promise as a prognostic biomarker and therapeutic target in ccRCC.","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2567815"},"PeriodicalIF":4.6,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12505508/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145238123","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

Challenges and caveats in manipulating extracellular vesicle secretion from pancreatic cancer cells. 控制胰腺癌细胞外囊泡分泌的挑战和注意事项。

IF 4.6 4区医学

Cancer Biology & Therapy Pub Date : 2025-12-31 Epub Date: 2025-10-25 DOI: 10.1080/15384047.2025.2569946

Jennifer M Finan, Jonathan R Brody

{"title":"Challenges and caveats in manipulating extracellular vesicle secretion from pancreatic cancer cells.","authors":"Jennifer M Finan, Jonathan R Brody","doi":"10.1080/15384047.2025.2569946","DOIUrl":"https://doi.org/10.1080/15384047.2025.2569946","url":null,"abstract":"Background: Extracellular vesicle (EV) signaling is important in multiple malignancies, including pancreatic ductal adenocarcinoma (PDAC). In this coordinated cell‒cell signaling mechanism, genetically altered tumor cells signal to surrounding normal cells to promote tumor progression. Many efforts have been made to mechanistically interrogate this signaling axis by inhibiting EV secretion from cells. These techniques leverage our understanding of how EV biogenesis interferes with ceramide production or GTPase activity, which aids in membrane fusion with the plasma membrane.Material and methods: Our group leveraged these methods in our orthotopic PDAC mouse model to investigate the importance of PDAC EV secretion. We interfered with the GTPases Rab27a and Rab35 and utilized an inhibitor of ceramide production (GW4869) to ablate EV secretion.Results and conclusion: Overall, we found that these models did not perform as anticipated, and we could not consistently inhibit KPC cell EV secretion. These results emphasize the challenges of interfering with EV secretion, as several parallel pathways, such as direct membrane budding, can compensate. Further studies are needed to develop models for studying the role of EVs in vivo.","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2569946"},"PeriodicalIF":4.6,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145367539","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

Sigma1 inhibitor suppression of adaptive immune resistance mechanisms mediated by cancer cell derived extracellular vesicles. Sigma1 抑制剂抑制由癌细胞衍生的细胞外囊泡介导的适应性免疫抵抗机制。

IF 4.4 4区医学

Cancer Biology & Therapy Pub Date : 2025-12-01 Epub Date: 2025-01-26 DOI: 10.1080/15384047.2025.2455722

Paola A Castagnino, Derick A Haas, Luca Musante, Nathalia A Tancler, Bach V Tran, Rhonda Kean, Alexandra R Steck, Luis A Martinez, Elahe A Mostaghel, D Craig Hooper, Felix J Kim

{"title":"Sigma1 inhibitor suppression of adaptive immune resistance mechanisms mediated by cancer cell derived extracellular vesicles.","authors":"Paola A Castagnino, Derick A Haas, Luca Musante, Nathalia A Tancler, Bach V Tran, Rhonda Kean, Alexandra R Steck, Luis A Martinez, Elahe A Mostaghel, D Craig Hooper, Felix J Kim","doi":"10.1080/15384047.2025.2455722","DOIUrl":"10.1080/15384047.2025.2455722","url":null,"abstract":"Adaptive immune resistance in cancer describes the various mechanisms by which tumors adapt to evade anti-tumor immune responses. IFN-γ induction of programmed death-ligand 1 (PD-L1) was the first defined and validated adaptive immune resistance mechanism. The endoplasmic reticulum (ER) is central to adaptive immune resistance as immune modulatory secreted and integral membrane proteins are dependent on ER. Sigma1 is a unique ligand-regulated integral membrane scaffolding protein enriched in the ER of cancer cells. PD-L1 is an integral membrane glycoprotein that is translated into the ER and processed through the cellular secretory pathway. At the cell surface, PD-L1 is an immune checkpoint molecule that binds PD-1 on activated T-cells and blocks anti-tumor immunity. PD-L1 can also be incorporated into cancer cell-derived extracellular vesicles (EVs), and EV-associated PD-L1 can inactivate T-cells within the tumor microenvironment. Here, we demonstrate that a selective small molecule inhibitor of Sigma1 can block IFN-γ mediated adaptive immune resistance in part by altering the incorporation of PD-L1 into cancer cell-derived EVs. Sigma1 inhibition blocked post-translational maturation of PD-L1 downstream of IFN-γ/STAT1 signaling. Subsequently, EVs released in response to IFN-γ stimulation were significantly less potent suppressors of T-cell activation. These results suggest that by reducing tumor derived immune suppressive EVs, Sigma1 inhibition may promote antitumor immunity. Sigma1 modulation presents a novel approach to regulating the tumor immune microenvironment by altering the content and production of EVs. Altogether, these data support the notion that Sigma1 may play a role in adaptive immune resistance in the tumor microenvironment.","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2455722"},"PeriodicalIF":4.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11776462/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143037220","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

β-amino acid substitution in the SIINFEKL antigen alters immunological recognition. SIINFEKL抗原中的β-氨基酸取代改变了免疫识别。

IF 4.4 4区医学

Cancer Biology & Therapy Pub Date : 2025-12-01 Epub Date: 2025-04-08 DOI: 10.1080/15384047.2025.2486141

Ichwaku Rastogi, John A Mannone, Ruslan Gibadullin, Jena E Moseman, John Sidney, Alessandro Sette, Douglas G McNeel, Samuel H Gellman

{"title":"β-amino acid substitution in the SIINFEKL antigen alters immunological recognition.","authors":"Ichwaku Rastogi, John A Mannone, Ruslan Gibadullin, Jena E Moseman, John Sidney, Alessandro Sette, Douglas G McNeel, Samuel H Gellman","doi":"10.1080/15384047.2025.2486141","DOIUrl":"10.1080/15384047.2025.2486141","url":null,"abstract":"Background: Peptide vaccines offer a direct way to initiate an immunogenic response to a defined antigen epitope. However, peptide vaccines are unstable in vivo, subject to rapid enzymatic proteolysis. Replacement of an α-amino acid residue with a homologous β-amino acid residue (native side chain, but backbone extended by a single CH2 unit) impairs proteolysis at nearby amide bonds. Therefore, antigen analogues containing α-to-β replacements have been examined for functional mimicry of native all-α antigens. Another group previously took this approach in the ovalbumin (OVA) antigen model by evaluating single α-to-β analogues of the murine major histocompatibility complex (MHC) I-restricted peptide SIINFEKL.Methods: We re-examined this set of α/β SIINFEKL antigens. We tested the susceptibility to proteolysis in mouse serum and their ability to activate OVA-antigen-specific CD8 T cells in vitro. Additionally, we tested the α/β antigens in vivo for their ability to induce an antigen-specific immunogenic response in naïve mice and in OVA-expressing tumor-bearing mice.Results: The α/β antigens were comparable to the native antigen in their susceptibility to proteolysis in serum. Each α/β antigen was capable of activating antigen-specific CD8 T cells in vitro. However, antigen-specific CD8 T cells induced against α/β antigens in vivo were not cross-reactive to the native antigen. Moreover, immunization with α/β analogues did not elicit anti-tumor effects in tumor-bearing mice.Conclusions: We conclude that even though α/β analogues of the SIINFEKL antigen can elicit a T cell-based response, this class of backbone-modified peptides is not promising from the perspective of antitumor vaccine development.","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2486141"},"PeriodicalIF":4.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11988276/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143810527","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

Fractionated radiotherapy initiated at the early stage of bone metastasis is effective to prolong survival in mouse model. 骨转移早期分次放疗可有效延长小鼠生存期。

IF 4.4 4区医学

Cancer Biology & Therapy Pub Date : 2025-12-01 Epub Date: 2025-01-20 DOI: 10.1080/15384047.2025.2455756

Yun Zhang, Zhunyi Gao, Ziwei Qi, Jiahe Xu, Jiao Xue, Lujie Xiong, Junhui Wang, Yuhui Huang, Songbing Qin

{"title":"Fractionated radiotherapy initiated at the early stage of bone metastasis is effective to prolong survival in mouse model.","authors":"Yun Zhang, Zhunyi Gao, Ziwei Qi, Jiahe Xu, Jiao Xue, Lujie Xiong, Junhui Wang, Yuhui Huang, Songbing Qin","doi":"10.1080/15384047.2025.2455756","DOIUrl":"10.1080/15384047.2025.2455756","url":null,"abstract":"Background and purpose: Bone metastasis is common for breast cancer and associated with poor prognosis. Currently, radiotherapy (RT) serves as the standard treatment for patients exhibiting symptoms of bone metastasis to alleviate pain. Whether earlier application of RT will better control bone metastasis remains unclear.Methods: We utilized a mouse model of breast cancer bone metastasis by intra-femoral injection of 4T1-luc breast tumor cells. The bone metastasis was treated by RT using various doses, timings, and modalities. Tumor growth was assessed through bioluminescence imaging, and lung metastases was quantified following lung tissue fixation. Flow cytometry was employed to analyze alterations in immune cell populations.Results: Single high-dose RT suppressed tumor growth of bone metastases, but caused severe side effects. Conversely, fractionated RT mitigated tumor growth in bone metastases with fewer adverse effects. Fractioned RT initiated at the early stage of bone metastasis effectively inhibited tumor growth in the bone, suppressed secondary lung metastases, and prolonged mouse survival. In line with the known pro- and anti-metastatic effects of neutrophils and T cells in breast cancer, respectively, earlier fractioned RT consistently decreased the proportions of neutrophils while increased the proportions of T cells in both the bone and the lung tissues.Conclusion: The data suggest that fractionated RT can inhibit the progression of early stage of bone metastasis and reduce secondary lung metastasis, leading to favorable outcomes. Therefore, these findings provide preclinical evidence to support the application of fractionated RT to treat patients with bone metastasis as earlier as possible.","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2455756"},"PeriodicalIF":4.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143000910","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

Correction. 修正。

IF 4.4 4区医学

Cancer Biology & Therapy Pub Date : 2025-12-01 Epub Date: 2025-05-14 DOI: 10.1080/15384047.2025.2500190

引用次数: 0

Daurisoline inhibits glycolysis of lung cancer by targeting the AKT-HK2 axis. Daurisoline通过靶向AKT-HK2轴抑制肺癌糖酵解。

IF 4.4 4区医学

Cancer Biology & Therapy Pub Date : 2025-12-01 Epub Date: 2024-12-19 DOI: 10.1080/15384047.2024.2442556

Shi-Ming Tan, Lan Luo, Yi-Fu He, Wei Li, Xin-Xing Wan

引用次数: 0