Cancer letters最新文献_第7页

A PP2A-mtATR-tBid axis links DNA damage-induced CIP2A degradation to apoptotic dormancy and therapeutic resistance in PDAC PP2A-mtATR-tBid轴将DNA损伤诱导的CIP2A降解与PDAC的凋亡休眠和治疗抗性联系起来。

IF 9.1 1区医学

Cancer letters Pub Date : 2025-05-10 DOI: 10.1016/j.canlet.2025.217790

Yibo Luo, Himadri Biswas, Yetunde Makinwa, Shi-He Liu, Zizheng Dong, Jing-Yuan Liu, Jian-Ting Zhang, Yue Zou

{"title":"A PP2A-mtATR-tBid axis links DNA damage-induced CIP2A degradation to apoptotic dormancy and therapeutic resistance in PDAC","authors":"Yibo Luo, Himadri Biswas, Yetunde Makinwa, Shi-He Liu, Zizheng Dong, Jing-Yuan Liu, Jian-Ting Zhang, Yue Zou","doi":"10.1016/j.canlet.2025.217790","DOIUrl":"10.1016/j.canlet.2025.217790","url":null,"abstract":"<div><div>DNA damage-based drugs are widely used in cancer therapy, yet resistance remains a major challenge. In this study, we uncovered a non-DNA repair mechanism contributing to resistance in pancreatic ductal adenocarcinoma (PDAC). We show that in gemcitabine-resistant PDAC cells, CIP2A undergoes ubiquitin-mediated degradation, resulting in enhanced PP2A phosphatase activity. This leads to the dephosphorylation of ATR at Ser428 in the cytoplasm, promoting the formation of the prolyl <em>cis</em>-isomeric form of ATR at its Ser428-Pro429 motif. The resulting <em>cis</em>-ATR functions as a mitochondria-targeted antiapoptotic protein (mtATR). Surprisingly, resistant PDAC cells paradoxically accumulated both mtATR and proapoptotic tBid at the mitochondria, forming a stable mtATR-tBid complex that induces a state of apoptotic dormancy. Disrupting this complex, either with the PP2A inhibitor LB-100 or a cytoplasmic ATR-specific antibody, reactivates the pre-accumulated tBid and restores apoptosis in resistant PDAC cells. In an orthotopic PDAC mouse model, LB-100 alone significantly inhibit gemcitabine-resistant tumor growth by disrupting the mtATR-tBid complex. These findings reveal a previously unrecognized mechanism of resistance to DNA damage-based therapies and identify a novel action mechanism of LB-100, characterized by the CIP2A degradation-mediated PP2A-mtATR-tBid axis. By targeting mtATR-tBid-mediated apoptotic dormancy, this strategy offers a promising approach to restore apoptotic sensitivity in drug-resistant cancers.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"627 ","pages":"Article 217790"},"PeriodicalIF":9.1,"publicationDate":"2025-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143975143","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Corrigendum to “CircMFN2/miR-361-3p/ELK1 feedback loop promotes glutaminolysis and the progression of hepatocellular carcinoma” [Cancer Lett. 614 (2025) 217473] “CircMFN2/miR-361-3p/ELK1反馈回路促进谷氨酰胺溶解和肝细胞癌的进展”的勘误表[Cancer Lett] . 614 (2025) 217473]

IF 9.1 1区医学

Cancer letters Pub Date : 2025-05-10 DOI: 10.1016/j.canlet.2025.217755

Xiaopei Hao , Xiangjun Qian , Chenxi Xie , Zhengzheng Wang , Xiaoqian Wang , Yang Ji , Xiaokai Zhang , Qingjun Li , Baishun Wan , Hong Cui , Li Wang , Nanmu Yang , Liang Qiao , Haibo Yu , Feng Han , Hao Zhuang , Jinxue Zhou

引用次数: 0

Targeting of COPⅠ elicits CD8+ T cell-mediated anti-tumor immunity and suppresses growth of intrahepatic cholangiocarcinoma

IF 9.1 1区医学

Cancer letters Pub Date : 2025-05-08 DOI: 10.1016/j.canlet.2025.217786

Zehong Chen , Guiqin Xu , Chen Xu , Yun Liu , Zhaojuan Yang , Lvzhu Xiang , You Zuo , Ningqian Zheng , Zhiqian Ye , Wangjie Xu , Yingbin Liu , Yongzhong Liu , Li Zhang

{"title":"Targeting of COPⅠ elicits CD8+ T cell-mediated anti-tumor immunity and suppresses growth of intrahepatic cholangiocarcinoma","authors":"Zehong Chen , Guiqin Xu , Chen Xu , Yun Liu , Zhaojuan Yang , Lvzhu Xiang , You Zuo , Ningqian Zheng , Zhiqian Ye , Wangjie Xu , Yingbin Liu , Yongzhong Liu , Li Zhang","doi":"10.1016/j.canlet.2025.217786","DOIUrl":"10.1016/j.canlet.2025.217786","url":null,"abstract":"<div><div>Intrahepatic cholangiocarcinoma (iCCA) possesses the immunosuppressive tumor microenvironment (TME) that limits the effectiveness of immunotherapy. Genetic alterations of the coat protein complex Ⅰ (COPⅠ) lead to STING activation and inflammatory immune response. This study aims to address whether targeting COPⅠ can be exploited as a strategy to elicit immune response and inhibit iCCA progression. Here, we demonstrated that the COPⅠ subunits were highly expressed in human and mouse iCCA tissues. Genetic and pharmacological inhibition of COPⅠ suppressed growth of the mouse autochthonous iCCAs driven by activated oncogenes. Disruption of COPⅠ increased T cell presence in tumor environment and elicited anti-tumor T cell response through activating STING-type‐I interferon (IFN‐I) pathway. Neutralizing CD8<sup>+</sup> T cell or STING deletion efficiently counteracted the suppression of iCCA growth by targeting COPⅠ. In addition, the Wnt/β-catenin signaling was dramatically attenuated in tumor cells by STING activation in the context of COPⅠ disruption. Notably, targeting COPⅠ markedly potentiates the therapeutic efficacy of anti-PD-1 in suppressing iCCA growth. In conclusion, our study reveals that targeting COPⅠ effectively suppresses tumor growth by enhancing T cell presence and function in mouse iCCA. STING activation by COPⅠ inhibition dedicates the T cell control of iCCA growth. COPⅠ is a potential target for iCCA treatment.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"626 ","pages":"Article 217786"},"PeriodicalIF":9.1,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143942906","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Mechanistic insights into CLNS1A-mediated chemoresistance and tumor progression in non-small cell lung cancer clns1a介导的非小细胞肺癌化疗耐药和肿瘤进展的机制见解

IF 9.1 1区医学

Cancer letters Pub Date : 2025-05-07 DOI: 10.1016/j.canlet.2025.217783

Tong-You Wade Wei , Jiun-Yi Hsia , Tsung-Ying Yang , Yu-Xu Huang , Guo-Zhi Wang , Yi-Chung Liu , Yi-Wun Wang , Fangzhou He , Jo-Mei Maureen Chen , Guo-Jun Zhao , Ping-Chiang Lyu , Li-Jen Su , Shao-Chih Chiu , Chang-Tze Ricky Yu

{"title":"Mechanistic insights into CLNS1A-mediated chemoresistance and tumor progression in non-small cell lung cancer","authors":"Tong-You Wade Wei , Jiun-Yi Hsia , Tsung-Ying Yang , Yu-Xu Huang , Guo-Zhi Wang , Yi-Chung Liu , Yi-Wun Wang , Fangzhou He , Jo-Mei Maureen Chen , Guo-Jun Zhao , Ping-Chiang Lyu , Li-Jen Su , Shao-Chih Chiu , Chang-Tze Ricky Yu","doi":"10.1016/j.canlet.2025.217783","DOIUrl":"10.1016/j.canlet.2025.217783","url":null,"abstract":"<div><div>CLNS1A is a chloride channel protein and an essential component of the methylosome complex, which additionally comprises PRMT5 and MEP50. In this study, we investigated its contribution to lung cancer and its potential as a therapeutic target. Analysis of transcriptomic datasets and western blotting revealed that CLNS1A, PRMT5, and MEP50 were overexpressed in lung cancer tissues, with elevated CLNS1A expression correlating with poor patient survival. CLNS1A overexpression enhanced platinum clearance from cells, increased the IC<sub>50</sub> values for chemotherapy, and improved cell survival. Conversely, the knockdown of CLNS1A increased drug accumulation, reduced survival, and increased sensitivity to chemotherapy. The 3W mutant, a chloride channel-defective variant with steric hindrance at key bottleneck residues, impaired chloride ion transport, thereby reducing drug resistance, migration, and anchorage-independent growth. Mechanistically, CLNS1A promotes drug efflux through its chloride channel activity and activates the FAK-SRC-RAC1 pathway to enhance motility and clonogenicity. It also facilitates PRMT5-mediated RUVBL1 methylation to support anti-apoptotic DNA damage response signaling. <em>In vivo</em>, CLNS1A overexpression accelerated tumor growth and reduced survival, whereas CLNS1A knockdown sensitized tumors to cisplatin, enhancing therapeutic efficacy. These findings suggest that CLNS1A is a potential biomarker and therapeutic target, and its inhibition offers a strategy to overcome drug resistance and limit the metastatic progression of lung cancer.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"626 ","pages":"Article 217783"},"PeriodicalIF":9.1,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143977400","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Corrigendum to “Inhibition of the NF-κB pathway by nafamostat mesilate suppresses colorectal cancer growth and metastasis” [Cancer Lett. 380 (2016) 87–97] “纳莫他酯抑制NF-κB通路抑制结直肠癌的生长和转移”的更正[癌症通讯，380 (2016)87-97]

IF 9.1 1区医学

Cancer letters Pub Date : 2025-05-06 DOI: 10.1016/j.canlet.2025.217756

Yun-Xin Lu , Huai-Qiang Ju , Feng Wang , Le-Zong Chen , Qi-Nian Wu , Hui Sheng , Hai-Yu Mo , Zhi-Zhong Pan , Dan Xie , Tie-Bang Kang , Gong Chen , Jing-Ping Yun , Zhao-Lei Zeng , Rui-Hua Xu

引用次数: 0

Glycolytic enzyme PFKFB4 governs lipolysis by promoting de novo lipogenesis to drive the progression of hepatocellular carcinoma 糖酵解酶PFKFB4通过促进新生脂肪生成来控制脂肪分解，从而驱动肝细胞癌的进展

IF 9.1 1区医学

Cancer letters Pub Date : 2025-05-06 DOI: 10.1016/j.canlet.2025.217774

Shuo Zhou , Yao Liu , Ning Zhang , Linmao Sun , Changyong Ji , Tianming Cui , Qi Chu , Shugeng Zhang , Jiabei Wang , Lianxin Liu

{"title":"Glycolytic enzyme PFKFB4 governs lipolysis by promoting de novo lipogenesis to drive the progression of hepatocellular carcinoma","authors":"Shuo Zhou , Yao Liu , Ning Zhang , Linmao Sun , Changyong Ji , Tianming Cui , Qi Chu , Shugeng Zhang , Jiabei Wang , Lianxin Liu","doi":"10.1016/j.canlet.2025.217774","DOIUrl":"10.1016/j.canlet.2025.217774","url":null,"abstract":"<div><div>Hepatocellular carcinoma (HCC) is among the most aggressive malignancies, marked by high recurrence rates and limited treatment efficacy, especially in HBV-associated HCC (HBV-HCC). This subtype exhibits pronounced metabolic reprogramming, with lipid synthesis playing a pivotal role in driving tumor aggressiveness and therapeutic resistance. However, the molecular mechanisms underlying this metabolic shift remain unclear. In our study, analysis of the LIHC-TCGA database and comparisons between HCC tissues and adjacent peri-tumoral tissues revealed that 6-Phosphofructo-2-Kinase/Fructose-2,6-Biphosphatase 4 (PFKFB4) is significantly upregulated in HBV-HCC. Moreover, elevated PFKFB4 expression correlates with poorer prognosis and unfavorable overall survival among HBV-HCC patients. Functional assays demonstrated that PFKFB4 promotes HCC proliferation by enhancing glycolysis and de novo lipid synthesis. Notably, PFKFB4 not only increases glycolytic flux but also upregulates sterol regulatory element-binding protein 1 (SREBP1) expression via its enzymatic activity. Mechanistically, PFKFB4 suppresses phosphorylated AMP-activated protein kinase (p-AMPK) through enhanced aerobic glycolysis, which in turn stimulates the level of SREBP1. Collectively, these findings position PFKFB4 as a critical mediator of metabolic reprogramming in HBV-HCC and a promising therapeutic target.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"626 ","pages":"Article 217774"},"PeriodicalIF":9.1,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143927489","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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ADAMs contribute to triple negative breast cancer via mTORC1 pathway: targeting ADAM-mTOR axis improves efficacy ADAMs通过mTORC1通路参与三阴性乳腺癌：靶向ADAM-mTOR轴可提高疗效

IF 9.1 1区医学

Cancer letters Pub Date : 2025-05-06 DOI: 10.1016/j.canlet.2025.217775

Shuying Liu , Huiqin Chen , Mihai Gagea , Lorenzo Federico , Fan Zhang , Javier Gomez , Kim-Anh Do , William F. Symmans , Gabriel N. Hortobagyi , Gordon B. Mills , Ana M. Gonzalez-Angulo , Debasish Tripathy

{"title":"ADAMs contribute to triple negative breast cancer via mTORC1 pathway: targeting ADAM-mTOR axis improves efficacy","authors":"Shuying Liu , Huiqin Chen , Mihai Gagea , Lorenzo Federico , Fan Zhang , Javier Gomez , Kim-Anh Do , William F. Symmans , Gabriel N. Hortobagyi , Gordon B. Mills , Ana M. Gonzalez-Angulo , Debasish Tripathy","doi":"10.1016/j.canlet.2025.217775","DOIUrl":"10.1016/j.canlet.2025.217775","url":null,"abstract":"<div><div>Breast cancer is the most frequently diagnosed cancer globally and the second leading cause of cancer-related deaths in American women. Triple-negative breast cancer (TNBC) lacks estrogen receptor, progesterone receptor, and human epidermal growth factor receptor 2. Thus, fewer targeting therapies are available for this most aggressive subtype. The A Disintegrin and Metalloproteinase (ADAM) family plays a vital role in cancer pathophysiology. Previous studies focused on single ADAM members. However, none of these have entered into the clinical arena as diagnostics or therapeutics for breast cancer. In this study, we demonstrate the upregulation of a panel of ADAM members in TNBC, and overexpression of all the individual ADAMs tested are correlated with poor patient survival, making it unlikely that targeting a single ADAM member would be effective. Reverse-phase protein array and multiplexed immunofluorescence revealed that ADAM10/15/17 expression was associated with activated mTOR signaling. Individual knockdown of ADAM10, ADAM15, or ADAM17 modestly reduced mTOR signaling, cellular proliferation and survival. However, the concurrent knockdown of the three ADAMs drastically decreased mTOR signaling and cellular aggressiveness. Consistently, combined targeting of ADAMs and mTOR increased inhibitory efficacy compared to monotherapy in ADAM-mTOR-activated tumor growth and invasion in vitro and in immunodeficient and immunocompetent mice. These results establish a functional link between ADAMs and activation of mTOR signaling, suggesting the ADAM-mTOR axis as a therapeutic target and biomarker for ADAM-enriched TNBC and, potentially, other tumor lineages with high ADAM activity.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"626 ","pages":"Article 217775"},"PeriodicalIF":9.1,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143927488","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Sialic Acids: Sweet modulators fueling cancer cells and domesticating the tumor microenvironment 唾液酸：促进癌细胞和肿瘤微环境驯化的甜调节剂

IF 9.1 1区医学

Cancer letters Pub Date : 2025-05-06 DOI: 10.1016/j.canlet.2025.217773

Jialu Bai , Ruiling Xiao , Decheng Jiang , Xiyuan Luo , Yuemeng Tang , Ming Cui , Lei You , Yupei Zhao

{"title":"Sialic Acids: Sweet modulators fueling cancer cells and domesticating the tumor microenvironment","authors":"Jialu Bai , Ruiling Xiao , Decheng Jiang , Xiyuan Luo , Yuemeng Tang , Ming Cui , Lei You , Yupei Zhao","doi":"10.1016/j.canlet.2025.217773","DOIUrl":"10.1016/j.canlet.2025.217773","url":null,"abstract":"<div><div>Tumor microenvironment (TME) can shift towards either immune activation or immunosuppression, influenced by various factors. Recent studies have underscored the pivotal role of sialic acids, a group of monosaccharides with a 9-carbon backbone, in modulating the TME. Aberrant expression or abnormal addition of sialic acids to the surface of cancer cells and within the tumor stroma has been identified as a key contributor to tumor progression. Abnormal sialylation on cancer cell surfaces can inhibit apoptosis, enhance cell proliferation, and facilitate metastasis. Notably, recent findings suggest that dysregulated sialic acid expression in the TME actively contributes to shaping an immunosuppressive niche by reducing the population of anti-tumor immune cells and impairing immune cell function. The mechanisms by which sialic acids foster immune escape and shape the immunosuppressive TME have been partially unraveled, particularly through interactions with sialic acid receptors on immune cells. Importantly, several sialic acid-targeted therapies are currently advancing into clinical trials, offering promising prospects for clinical translation. This dysregulated sialylation represents a significant opportunity for molecular diagnostics and therapeutic interventions in oncology. Targeting aberrant sialylation or disrupting the interaction between sialic acids and their receptors offers potential strategies to reprogram the TME towards an anti-tumor phenotype, thereby facilitating the advancement of innovative cancer therapies.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"626 ","pages":"Article 217773"},"PeriodicalIF":9.1,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143932070","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Macrophage polarization in cancer and beyond: from inflammatory signaling pathways to potential therapeutic strategies 巨噬细胞极化在癌症及其他：从炎症信号通路到潜在的治疗策略

IF 9.1 1区医学

Cancer letters Pub Date : 2025-05-03 DOI: 10.1016/j.canlet.2025.217772

Xiao Bai , Yun-Ran Guo , Zhe-Ming Zhao , Xin-Yun Li , Dong-Qiu Dai , Jia-Kui Zhang , Yong-Shuang Li , Chun-Dong Zhang

{"title":"Macrophage polarization in cancer and beyond: from inflammatory signaling pathways to potential therapeutic strategies","authors":"Xiao Bai , Yun-Ran Guo , Zhe-Ming Zhao , Xin-Yun Li , Dong-Qiu Dai , Jia-Kui Zhang , Yong-Shuang Li , Chun-Dong Zhang","doi":"10.1016/j.canlet.2025.217772","DOIUrl":"10.1016/j.canlet.2025.217772","url":null,"abstract":"<div><div>Macrophages are innate immune cells distributed throughout the body that play vital roles in organ development, tissue homeostasis, and immune surveillance. Macrophages acquire a binary M1/M2 polarized phenotype through signaling cascades upon sensing different signaling molecules in the environment, thereby playing a core role in a series of immune tasks, rendering precise regulation essential. M1/M2 macrophage phenotypes regulate inflammatory responses, while controlled activation of inflammatory signaling pathways is involved in regulating macrophage polarization. Among the relevant signaling pathways, we focus on the six well-characterized NF-κB, MAPK, JAK-STAT, PI3K/AKT, inflammasome, and cGAS-STING inflammatory pathways, and elucidate their roles and crosstalk in macrophage polarization. Furthermore, the effects of many environmental signals that influence macrophage polarization are investigated by modulating these pathways <em>in vivo</em> and <em>in vitro</em>. We thus detail the physiological and pathophysiological status of these six inflammatory signaling pathways and involvement in regulating macrophage polarization in cancer and beyond, as well as describe potential therapeutic approaches targeting these signaling pathways. In this review, the latest research advances in inflammatory signaling pathways regulating macrophage polarization are reviewed, as targeting these inflammatory signaling pathways provides suitable strategies to intervene in macrophage polarization and various tumor and non-tumor diseases.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"625 ","pages":"Article 217772"},"PeriodicalIF":9.1,"publicationDate":"2025-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143922472","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Colorectal cancer peritoneal metastasis is promoted by tissue-specific fibroblasts that can arise in response to various local disorders 结直肠癌腹膜转移是由组织特异性成纤维细胞促进的，这种成纤维细胞可以在各种局部疾病的反应中产生

IF 9.1 1区医学

Cancer letters Pub Date : 2025-05-02 DOI: 10.1016/j.canlet.2025.217749

Raffaele Strippoli

引用次数: 0