Neoplasia最新文献

{"title":"Establishment of patient-derived 3D in vitro models of sarcomas: literature review and guidelines on behalf of the FORTRESS working group","authors":"Lore De Cock ,&nbsp;Ieva Palubeckaitė ,&nbsp;Francesca Bersani ,&nbsp;Tobias Faehling ,&nbsp;Sandro Pasquali ,&nbsp;Sam Umbaugh ,&nbsp;Michael Torsten Meister ,&nbsp;Molly R. Danks ,&nbsp;Piotr Manasterski ,&nbsp;Richard Miallot ,&nbsp;Manuela Krumbholz ,&nbsp;Siyer Roohani ,&nbsp;Dominique Heymann ,&nbsp;Florencia Cidre-Aranaz ,&nbsp;Agnieszka Wozniak ,&nbsp;Patrick Schöffski ,&nbsp;Judith V.M.G. Bovée ,&nbsp;Alessandra Merlini ,&nbsp;Sanne Venneker","doi":"10.1016/j.neo.2025.101171","DOIUrl":"10.1016/j.neo.2025.101171","url":null,"abstract":"<div><div>Sarcomas are a large family of rare and heterogeneous mesenchymal tumors, which respond poorly to available systemic treatments. Translation of preclinical findings into clinical applications has been slow, limiting improvements in patients’ outcomes and ultimately highlighting the need for a better understanding of sarcoma biology to develop more effective, subtype-specific therapies. To this end, reliable preclinical models are crucial, but the development of 3D <em>in vitro</em> sarcoma models has been lagging behind that of epithelial cancers. This is primarily due to the rarity and heterogeneity of sarcomas, and lack of widespread knowledge regarding the optimal growth conditions of these <em>in vitro</em> models. In this review, we provide an overview of currently available sarcoma tumoroid models, together with guidelines and suggestions for model development and characterization, on behalf of the FORTRESS (Forum For Translational Research in Sarcomas) international research working group on 3D sarcoma models.</div></div>","PeriodicalId":18917,"journal":{"name":"Neoplasia","volume":"65 ","pages":"Article 101171"},"PeriodicalIF":4.8,"publicationDate":"2025-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143901959","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DNA-methylation eraser TET2 activates WTIP expression to suppress an AKT-dependent chemoresistance of gastric cancer","authors":"Yan Guo ,&nbsp;Hongyang Yu ,&nbsp;Jinyang Li ,&nbsp;Kewei Liu ,&nbsp;Mengyi Han ,&nbsp;Yuxin Tang ,&nbsp;Li Su ,&nbsp;Xianfeng Li ,&nbsp;Haixia Wu ,&nbsp;Dongfeng Chen","doi":"10.1016/j.neo.2025.101166","DOIUrl":"10.1016/j.neo.2025.101166","url":null,"abstract":"<div><div>Chemoresistance is one of the major causes of the failure in gastric cancer (GC) treatment and leads to poor clinical outcomes. Ten-eleven translocation (TET) 2 expression and activity are frequently reduced in solid tumors. However, whether TET2 participants in GC chemoresistance remains poorly understood. In this study, we demonstrated that the TET2 acts as a novel suppressor of GC chemoresistance. TET2 and transcription factor PATZ1 work together to promote the expression of WTIP. WTIP interacts with PP2A to inhibit the T308 phosphorylation and kinase activity of AKT, thereby suppressing stemness and chemoresistance of GC. Thus, the novel TET2-WTIP transcriptional axis, which is frequently silenced, suppresses an AKT-dependent chemoresistance of GC. TET2, combined with WTIP and AKT-pT308, can synergistically serve as a biomarker for predicting chemotherapy response in GC patients. Furthermore, we highlight that combining AKT inhibitor with chemotherapy is a promising therapeutic strategy for TET2-silenced GCs with chemoresistance in clinic.</div></div>","PeriodicalId":18917,"journal":{"name":"Neoplasia","volume":"65 ","pages":"Article 101166"},"PeriodicalIF":4.8,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143869185","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “PRMT1 methylates METTL14 to modulate its oncogenic function” [Neoplasia 42 (2023) 100912]","authors":"Jingchao Wang ,&nbsp;Zhen Wang ,&nbsp;Hiroyuki Izunuka ,&nbsp;Wenyi Wei ,&nbsp;Jing Liu","doi":"10.1016/j.neo.2025.101167","DOIUrl":"10.1016/j.neo.2025.101167","url":null,"abstract":"","PeriodicalId":18917,"journal":{"name":"Neoplasia","volume":"65 ","pages":"Article 101167"},"PeriodicalIF":4.8,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143863890","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An antibody targeting an immune checkpoint molecule BTN2A2 enhances anti-tumor immunity","authors":"Li Xiao ,&nbsp;Rong Hu ,&nbsp;Wei Chen ,&nbsp;Jie Gao ,&nbsp;Youbo Zhao ,&nbsp;Zuli Wang ,&nbsp;Guangshi Du ,&nbsp;Yishen Tian ,&nbsp;Laijun Lai ,&nbsp;Lu Liu ,&nbsp;Min Su","doi":"10.1016/j.neo.2025.101161","DOIUrl":"10.1016/j.neo.2025.101161","url":null,"abstract":"<div><div>Tumors exploit immune checkpoints to evade immune responses. Therefore, targeting these checkpoints has become a key strategy in cancer immunotherapy. In this study, we have developed a novel immune checkpoint inhibitor (ICI) targeting the B7 family-related molecule BTN2A2. The human BTN2A2 protein, which was highly expressed in some tumor tissues and activated antigen-presenting cells (APCs), can inhibit T cell activation and proliferation. The anti-BTN2A2 monoclonal antibody (mAb) can neutralize the inhibitory effect of BTN2A2 on T cells. In mouse models of pancreatic cancer and glioma, compared to the control group, the anti-BTN2A2 treatment group exhibited tumor shrinkage of 35.8 % (<em>P</em> &lt; 0.05) and 51.2 % (<em>P</em> &lt; 0.01), respectively, along with increased CD8+ tumor-infiltrating lymphocytes (TILs) by 1.7-fold (<em>P</em> &lt; 0.001) and 2.2-fold (<em>P</em> &lt; 0.001), respectively. In addition, anti-BTN2A2 mAb also increased the infiltration of B cells, M1 macrophages, and the expression of inflammatory cytokines in T cells, while reducing the infiltration of M2 macrophages, myeloid-derived suppressor cells (MDSCs), and regulatory T cells (Tregs). Thus, anti-hBTN2A2 mAb normalizes the immunodeficient tumor microenvironment (TME) and inhibits tumor growth. Our results suggest that targeting the BTN2A2 immune checkpoint may represent a novel strategy for cancer treatment, especially in immunosuppressive 'cold' tumors.</div></div>","PeriodicalId":18917,"journal":{"name":"Neoplasia","volume":"65 ","pages":"Article 101161"},"PeriodicalIF":4.8,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143852228","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Activation of PERK/eIF2α/ATF4 signaling inhibits ERα expression in breast cancer","authors":"Yuanli Wu ,&nbsp;Gang Wang ,&nbsp;Ruixue Yang ,&nbsp;Duanfang Zhou ,&nbsp;Qingjuan Chen ,&nbsp;Qiuya Wu ,&nbsp;Bo Chen ,&nbsp;Lie Yuan ,&nbsp;Na Qu ,&nbsp;Hongmei Wang ,&nbsp;Moustapha Hassan ,&nbsp;Ying Zhao ,&nbsp;Mingpu Liu ,&nbsp;Zhengze Shen ,&nbsp;Weiying Zhou","doi":"10.1016/j.neo.2025.101165","DOIUrl":"10.1016/j.neo.2025.101165","url":null,"abstract":"<div><div>Approximately 70–80% of breast cancers rely on estrogen receptor alpha (ERα) for growth. The unfolded protein response (UPR), a cellular response to endoplasmic reticulum stress (ERS), is an important process crucial for oncogenic transformation. The effect of ERS on ERα expression and signaling remains incompletely elucidated. Here, we focused on the regulatory mechanisms of ERS on ERα expression in ER-positive breast cancer (ER+ BC). Our results demonstrate that ERα protein and mRNA levels in ER+ BC cells are considerably reduced by the ERS inducers thapsigargin (TG) and brefeldin A (BFA) via the PERK/eIF2α/ATF4 signaling pathway. ChIP-qPCR and luciferase reporter gene analysis revealed that ERS induction facilitated ATF4 binding to the <em>ESR1</em> (the gene encoding ERα) promoter region, thereby suppressing <em>ESR1</em> promoter activity and inhibiting ERα expression. Furthermore, selective activation of PERK signaling or ATF4 overexpression attenuated ERα expression and tumor cell growth both <em>in vitro</em> and <em>in vivo</em>. In conclusion, our results demonstrate that ERS suppresses ERα expression transcriptionally via the PERK/eIF2α/ATF4 signaling. Our study provides insights into the treatment of ER+ BC by targeting ERα signaling through selective activation of the PERK branch of the UPR.</div></div>","PeriodicalId":18917,"journal":{"name":"Neoplasia","volume":"65 ","pages":"Article 101165"},"PeriodicalIF":4.8,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143847538","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Establishing a comprehensive panel of patient-derived xenograft models for high-grade endometrial carcinoma: molecular subtypes, genetic alterations, and therapeutic target profiling","authors":"Sho Sato ,&nbsp;Shigehiro Yagishita ,&nbsp;Hiroshi Yoshida ,&nbsp;Daisuke Shintani ,&nbsp;Aiko Ogasawara ,&nbsp;Tadaaki Nishikawa ,&nbsp;Masanori Yasuda ,&nbsp;Keiji Furuuchi ,&nbsp;Toshimitsu Uenaka ,&nbsp;Akinobu Hamada ,&nbsp;Kosei Hasegawa","doi":"10.1016/j.neo.2025.101158","DOIUrl":"10.1016/j.neo.2025.101158","url":null,"abstract":"<div><h3>Background</h3><div>High-grade endometrial cancer (EC) has a poor prognosis, but molecular classification-based treatments present new therapeutic opportunities. Antibody-drug conjugates (ADC) emerge as promising tools, yet a deeper understanding of antigen dynamics, optimal therapeutic sequencing, and resistance mechanisms is essential. This study investigates the utility of patient-derived xenograft (PDX) models for EC as preclinical platforms, evaluating molecular subtypes and the ADC targets expression of patient and PDX tumors.</div></div><div><h3>Methods</h3><div>We developed a comprehensive panel of molecularly characterized PDX models from patients with EC representing various histological types. Molecular subtypes and gene alterations were analyzed using sequencing and immunohistochemistry. ADC targets, including human epidermal growth factor receptor 2, trophoblast cell-surface antigen 2, B7-H4, folate receptor alpha, and cadherin-6, were profiled.</div></div><div><h3>Results</h3><div>Thirty-one EC-PDX models were successfully established, maintaining histological fidelity and 93.1 % molecular subtype consistency with the patient tumors. Notably, 80.6 % of the PDX models exhibited high expression (2+/3+) of at least one ADC target, and 54.8 % displayed high expression of multiple targets. Remarkably, 9.7 % showed high expression of all targets, with gene mutations also characterized. Meanwhile, patient tumors, 78.8 % showed high expression (2+/3+) of at least one ADC target, and 63.6 % showed high expression of multiple targets.</div></div><div><h3>Conclusion</h3><div>The molecularly classified EC-PDX panel, enriched with detailed antigen profiles and genetic data, provides a robust platform for investigating novel ADC therapies and precision treatment strategies for high-grade EC.</div></div>","PeriodicalId":18917,"journal":{"name":"Neoplasia","volume":"64 ","pages":"Article 101158"},"PeriodicalIF":4.8,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143785273","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Systemic inflammation in response to radiation drives the genesis of an immunosuppressed tumor microenvironment","authors":"Lin Ma ,&nbsp;Jian-Hua Mao ,&nbsp;Mary Helen Barcellos-Hoff","doi":"10.1016/j.neo.2025.101164","DOIUrl":"10.1016/j.neo.2025.101164","url":null,"abstract":"<div><div>The composition of the tumor immune microenvironment has become a major determinant of response to therapy, particularly immunotherapy. Clinically, a tumor microenvironment lacking lymphocytes, so-called \"cold\" tumors, are considered poor candidates for immune checkpoint inhibition. In this review, we describe the diversity of the tumor immune microenvironment in breast cancer and how radiation exposure alters carcinogenesis. We review the development and use of a radiation-genetic mammary chimera model to clarify the mechanism by which radiation acts. Using the chimera model, we demonstrate that systemic inflammation elicited by a low dose of radiation is key to the construction of an immunosuppressive tumor microenvironment, resulting in aggressive, rapidly growing tumors lacking lymphocytes. Our experimental studies inform the non-mutagenic mechanisms by which radiation affects cancer and provide insight into the genesis of cold tumors.</div></div>","PeriodicalId":18917,"journal":{"name":"Neoplasia","volume":"64 ","pages":"Article 101164"},"PeriodicalIF":4.8,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143760019","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"L-methionine promotes CD8+ T cells killing hepatocellular carcinoma by inhibiting NR1I2/PCSK9 signaling","authors":"Chengsha Yuan ,&nbsp;Changpeng Hu ,&nbsp;Huyue Zhou,&nbsp;Wuyi Liu,&nbsp;Wenjing Lai,&nbsp;Yafeng Liu,&nbsp;Yue Yin,&nbsp;Guobing Li,&nbsp;Rong Zhang","doi":"10.1016/j.neo.2025.101160","DOIUrl":"10.1016/j.neo.2025.101160","url":null,"abstract":"<div><h3>Background</h3><div>Liver cancer has consistently high incidence and mortality rates among malignant tumors. PCSK9, a target for hypercholesterolemia therapy, has recently been identified as an inhibitor of anti-tumor immunity, and targeting PCSK9 effectively inhibits tumor progression. However, small molecule inhibitors are lacking due to its flat protein structure.</div></div><div><h3>Methods</h3><div>PCSK9 transcription inhibitor screening was conducted using a PCSK9 promoter-driven td-Tomato plasmid. Quantitative real-time PCR and immunoblotting were employed to assess the effect of L-methionine on PCSK9 expression in HCC cell lines. Co-culture experiments were performed to evaluate the impact of L-methionine on CD8⁺ T cell-mediated killing of liver cancer cells. RNA sequencing, CUT&amp;Tag, gene editing, and luciferase reporter assays were utilized to identify the transcription factor regulating PCSK9. Additionally, liver cancer xenograft and spontaneous liver cancer mouse models were used to evaluate the anti-cancer efficacy of L-methionine.</div></div><div><h3>Results</h3><div>Our study identified L-methionine, an essential amino acid, as a transcriptional inhibitor of PCSK9. The optimal dose of L-methionine to inhibit PCSK9 expression and enhance CD8⁺ T cell-mediated killing of liver cancer cells <em>in vitro</em> is 50 μM. Furthermore, intraperitoneal injection of 5 mg/kg/day of L-methionine significantly inhibited tumor growth in both liver cancer xenograft and spontaneous liver cancer mouse models. Mechanistically, we identified NR1I2 as a key transcription factor for PCSK9 and their crucial binding site was TGCACCCTGACAC. L-methionine inhibits PCSK9 transcription by downregulating NR1I2.</div></div><div><h3>Conclusions</h3><div>This work demonstrates that L-methionine promotes CD8⁺ T cell-mediated killing of hepatocellular carcinoma by inhibiting NR1I2/PCSK9 signaling. Our study introduces a novel and convenient approach to inhibit PCSK9 and provides a theoretical basis for the rational supplementation of L-methionine in liver cancer patients.</div></div>","PeriodicalId":18917,"journal":{"name":"Neoplasia","volume":"64 ","pages":"Article 101160"},"PeriodicalIF":4.8,"publicationDate":"2025-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143725300","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High dose acetaminophen re-polarizes CD11b+ cells in the tumor microenvironment towards an activated macrophage phenotype","authors":"Allyn Bryan ,&nbsp;Madison Isbell ,&nbsp;Pavani Pingali ,&nbsp;Lauren May ,&nbsp;Syed A. Shah ,&nbsp;Adam Khader ,&nbsp;Andrea Galabow ,&nbsp;Madelyn Lorenz ,&nbsp;Jennifer Koblinski ,&nbsp;Won Sok Lee ,&nbsp;Rebecca K Martin ,&nbsp;Bhaumik Patel ,&nbsp;Joseph Landry ,&nbsp;Alex Neuwelt","doi":"10.1016/j.neo.2025.101155","DOIUrl":"10.1016/j.neo.2025.101155","url":null,"abstract":"<div><h3>Objective</h3><div>High dose acetaminophen (AAP) has demonstrated promising results in early phase clinical trials for treatment of advanced malignancies. When administered concurrently with the CYP2E1 inhibitor fomepizole, AAP can be dose-escalated 100-fold relative to standard dosing without liver toxicity and without compromising anti-tumor activity.</div></div><div><h3>Methods and analysis</h3><div>The current study used a 23-plex flow cytometry panel to study AAP-induced changes in the tumor immune microenvironment of syngeneic mouse breast tumors. Effects of AAP on macrophage function and antigen presentation, alone and in combination with PD-1 antibodies, were evaluated.</div></div><div><h3>Results</h3><div>Findings demonstrated that the vast majority of CD45+ cells in the triple negative breast cancer model are CD11b+ cells of the innate immune system. The CD11b+ cells in the tumor micro-environment of vehicle-treated mice were mostly comprised of GR1+ myeloid derived suppressor cells. On the other hand, the CD11b+ cells in the high dose AAP-treated mice were mostly of the activated macrophage phenotype (F4/80+CD80+MHCII+). In vitro studies were performed to better understand AAP effects on macrophage function. It was demonstrated that AAP enhances phagocytosis as well as antigen presentation by macrophages to antigen-reactive T-cells. These effects are amplified when PD-1 antibodies are combined with AAP in the in vitro antigen presentation assay. Furthermore, AAP has synergistic anti-tumor activity in vivo when combined with PD-1 antibody therapy, an effect that is macrophage dependent.</div></div><div><h3>Conclusion</h3><div>The present study demonstrates profound AAP-induced changes in the tumor immune microenvironment including the differentiation of CD11b+ cells towards an activated “M1” macrophage phenotype.</div></div>","PeriodicalId":18917,"journal":{"name":"Neoplasia","volume":"64 ","pages":"Article 101155"},"PeriodicalIF":4.8,"publicationDate":"2025-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143734624","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MTFR1 phosphorylation-activated adaptive mitochondrial fusion is essential for colon cancer cell survival during glucose deprivation","authors":"Nan Zhang,&nbsp;Lu Dong,&nbsp;Sifan Liu,&nbsp;Tingting Ning,&nbsp;Shengtao Zhu","doi":"10.1016/j.neo.2025.101159","DOIUrl":"10.1016/j.neo.2025.101159","url":null,"abstract":"<div><h3>Background</h3><div>Mitochondrial dynamics are essential for maintaining cellular function under metabolic stress. However, their role in colon cancer's response to glucose deprivation remains poorly understood.</div></div><div><h3>Methods</h3><div>The role of the mitochondrial protein MTFR1 in colon cancer proliferation was evaluated using CCK-8 and colony formation assays. Mass spectrometry identified MTFR1-interacting proteins and phosphorylation sites. Mitochondrial morphology was examined with Mitotracker staining, and mitochondrial function was evaluated using MitoSOX, JC-1 staining, and the Seahorse cell mitochondrial stress test.</div></div><div><h3>Results</h3><div>We observed that MTFR1 is highly expressed in colon cancer cells and interacts with NEK1 under glucose deprivation. This interaction induces phosphorylation of MTFR1 at serine 119, which promotes mitochondrial fusion and supports mitochondrial function. Consequently, enhanced oxidative phosphorylation improves cellular tolerance to glucose deprivation.</div></div><div><h3>Conclusions</h3><div>Our findings highlight the importance of MTFR1 in modulating mitochondrial dynamics and its potential impact on colon cancer cell survival under metabolic stress. These results suggest that MTFR1 serine 119 could be a key regulator of colon cancer cell metabolism and a potential therapeutic target for enhancing cancer cell response to metabolic challenges.</div></div>","PeriodicalId":18917,"journal":{"name":"Neoplasia","volume":"63 ","pages":"Article 101159"},"PeriodicalIF":4.8,"publicationDate":"2025-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143682611","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}