Carcinogenesis最新文献_第9页

PPP1r18 promotes tumor progression in esophageal squamous cell carcinoma by regulating the calcineurin-mediated ERK pathway. PPP1r18 通过调节钙神经蛋白介导的 ERK 通路促进食管鳞状细胞癌的肿瘤进展。

IF 3.3 3区医学

Carcinogenesis Pub Date : 2024-09-11 DOI: 10.1093/carcin/bgae028

Changhao Ren, Linfeng Wu, Shaoyuan Zhang, Kangwei Qi, Yifei Zhang, Jiacheng Xu, Yuanyuan Ruan, Mingxiang Feng

{"title":"PPP1r18 promotes tumor progression in esophageal squamous cell carcinoma by regulating the calcineurin-mediated ERK pathway.","authors":"Changhao Ren, Linfeng Wu, Shaoyuan Zhang, Kangwei Qi, Yifei Zhang, Jiacheng Xu, Yuanyuan Ruan, Mingxiang Feng","doi":"10.1093/carcin/bgae028","DOIUrl":"10.1093/carcin/bgae028","url":null,"abstract":"Esophageal cancer is one of the most common malignant tumors, and the 5-year overall survival rate is only 20%. Esophageal squamous cell carcinoma (ESCC) is the primary histological type of esophageal carcinoma in China. Protein phosphatase 1 regulatory subunit 18 (PPP1r18) is one of the actin-regulatory proteins and is able to bind to protein phosphatase 1 catalytic subunit alpha (PPP1CA). Yet, little is known about the role of PPP1r18 in ESCC. This study aimed to elucidate the biological functions of PPP1r18 in the ESCC progression. Clinical samples first confirmed that PPP1r18 expression was upregulated in ESCC, and PPP1r18 was correlated with tumor invasion depth, lymph node metastasis, distant metastasis and reduced overall survival. We then observed that PPP1r18 overexpression enhanced cell proliferation in vitro and in vivo. Mechanistically, PPP1r18 regulated tumor progression of ESCC through activating the calcineurin-mediated ERK pathway, rather than binding to PPP1CA. Collectively, our results suggest that PPP1r18 promotes ESCC progression by regulating the calcineurin-mediated ERK pathway. PPP1r18 might be a potential target for the diagnosis and treatment of ESCC.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":"673-684"},"PeriodicalIF":3.3,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140875954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Sevoflurane inhibits lung cancer development by promoting FUS1 transcription via downregulating IRF6. 七氟烷通过下调IRF6促进FUS1转录，从而抑制肺癌发展

IF 3.3 3区医学

Carcinogenesis Pub Date : 2024-08-12 DOI: 10.1093/carcin/bgae034

Pei Zhou, Lei Yang, Xinyu Ma, Qiuguo Li

{"title":"Sevoflurane inhibits lung cancer development by promoting FUS1 transcription via downregulating IRF6.","authors":"Pei Zhou, Lei Yang, Xinyu Ma, Qiuguo Li","doi":"10.1093/carcin/bgae034","DOIUrl":"10.1093/carcin/bgae034","url":null,"abstract":"Lung cancer is a major contributor to cancer deaths worldwide and is on the rise. Although surgical resection has been widely used as a standard therapy for lung cancer patients, the relapse rate after surgery is high. It is still unclear whether there is a potential drug that can reduce the probability of postsurgical recurrence in lung cancer patients. We used 5 typical lung cancer cell lines as well as 41 lung cancer tissue samples and paracancer tissue samples to investigate the expression levels of interferon regulatory factor 6 (IRF6) and tumor suppressor candidate 2 (TUSC2, also known as FUS1). We also treated lung cancer cells (H322 and A549) with different concentrations of sevoflurane to study its influence on lung cancer cell tumorigenesis. Lentivirus-mediated gain-of-function studies of IRF6 and FUS1 were applied to validate the role of IRF6 and FUS1 in lung cancer. Next, we used short hairpin RNA-mediated loss of function of IRF6 and luciferase, chromatin immunoprecipitation assays to validate the regulatory role of IRF6 on FUS1. Our findings reported that IRF6 was upregulated in lung cancer tissues, while FUS1 was downregulated. Functional assays revealed that sevoflurane inhibits lung cancer development by downregulating IRF6 expression. Luciferase and chromatin immunoprecipitation-quantitative real-time PCR assays uncovered that IRF6 represses FUS1 transcriptional expression in lung cancer cells. We have shown that sevoflurane prevents lung cancer development by downregulating IRF6 to stimulate FUS1 transcription, indicating that sevoflurane can be used as the potential anesthetic drug in surgical resection to reduce postoperative tumor relapse in lung cancer patients.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":"543-555"},"PeriodicalIF":3.3,"publicationDate":"2024-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141178096","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Diverse functions of Tribbles homolog 3 in cancers and its potential as a therapeutic target. TRIB3 在癌症中的多种功能及其作为治疗靶点的潜力。

IF 3.3 3区医学

Carcinogenesis Pub Date : 2024-08-12 DOI: 10.1093/carcin/bgae042

Shiying Lei, Jiajun Sun, Yifang Xie, Xiaojuan Xiao, Xiaofeng He, Sheng Lin, Huifang Zhang, Zineng Huang, Haiqin Wang, Xusheng Wu, Hongling Peng, Jing Liu

{"title":"Diverse functions of Tribbles homolog 3 in cancers and its potential as a therapeutic target.","authors":"Shiying Lei, Jiajun Sun, Yifang Xie, Xiaojuan Xiao, Xiaofeng He, Sheng Lin, Huifang Zhang, Zineng Huang, Haiqin Wang, Xusheng Wu, Hongling Peng, Jing Liu","doi":"10.1093/carcin/bgae042","DOIUrl":"10.1093/carcin/bgae042","url":null,"abstract":"Currently, cancer is the second leading cause of death worldwide, and potential targeted drugs and molecular pathways for cancer development and progression have been a hot research topic worldwide. In recent years, the importance of the kinase superfamily in diseases has been well demonstrated by studies on various molecular mechanisms of kinases and the successful application of their inhibitors in diseases. Pseudokinases are members of the kinase superfamily, which have been increasingly documented to play a crucial role in cancers year after year. As a member of pseudokinases, tribbles homolog 3 (TRIB3) also exerts diverse functions in different cancers through different interacting proteins and molecular pathways, especially in tumor immunity, stemness, drug resistance, metabolism, and autophagy. In addition, peptide drugs targeting TRIB3 have high specificity in preclinical studies, which shows great promise for TRIB3 application in diseases including cancers. In this review, we dissect diverse functions played by TRIB3 in different cancers, describing the underlying mechanisms in detail. Notably, inhibitors and agonists currently available for TRIB3 are discussed, indicating the potential for TRIB3 as a therapeutic target.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":"527-542"},"PeriodicalIF":3.3,"publicationDate":"2024-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141431485","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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 to: CRL4DCAF4 E3 ligase-mediated degradation of MEN1 transcriptionally reactivates hTERT to sustain immortalization in colorectal cancer cells. 更正为CRL4DCAF4 E3连接酶介导的MEN1转录降解可重新激活hTERT，维持结直肠癌细胞的永生化。

IF 3.3 3区医学

Carcinogenesis Pub Date : 2024-08-12 DOI: 10.1093/carcin/bgae039

引用次数: 0

CacyBP promotes the development of lung adenocarcinoma by regulating OTUD5. CacyBP 通过调控 OTUD5 促进肺腺癌的发展。

IF 3.3 3区医学

Carcinogenesis Pub Date : 2024-08-12 DOI: 10.1093/carcin/bgae023

Mixue Bai, Kun Lu, Yingying Che, Lin Fu

{"title":"CacyBP promotes the development of lung adenocarcinoma by regulating OTUD5.","authors":"Mixue Bai, Kun Lu, Yingying Che, Lin Fu","doi":"10.1093/carcin/bgae023","DOIUrl":"10.1093/carcin/bgae023","url":null,"abstract":"Lung cancer is the most common and lethal malignancy, with lung adenocarcinoma accounting for approximately 40% of all cases. Despite some progress in understanding the pathogenesis of this disease and developing new therapeutic approaches, the current treatments for lung adenocarcinoma remain ineffective due to factors such as high tumour heterogeneity and drug resistance. Therefore, there is an urgent need to identify novel therapeutic targets. Calcyclin-binding protein (CacyBP) can regulate a variety of physiological processes by binding to different proteins, but its function in lung adenocarcinoma is unknown. Here, we show that CacyBP is highly expressed in lung adenocarcinoma tissues, and high CacyBP expression correlates with poorer patient survival. Moreover, overexpression of CacyBP promoted the proliferation, migration and invasion of lung adenocarcinoma cell lines. Further mechanistic studies revealed that CacyBP interacts with the tumour suppressor ovarian tumour (OTU) deubiquitinase 5 (OTUD5), enhances the ubiquitination and proteasomal degradation of OTUD5 and regulates tumourigenesis via OTUD5. In conclusion, our study reveals a novel mechanism by which CacyBP promotes tumourigenesis by increasing the ubiquitination level and proteasome-dependent degradation of OTUD5, providing a potential target for the treatment of lung adenocarcinoma.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":"595-606"},"PeriodicalIF":3.3,"publicationDate":"2024-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140334839","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

TMEM16A inhibits autophagy and promotes the invasion of hypopharyngeal squamous cell carcinoma through mTOR pathway. TMEM16A 可抑制自噬，并通过 mTOR 通路促进下咽鳞状细胞癌的侵袭。

IF 3.3 3区医学

Carcinogenesis Pub Date : 2024-08-12 DOI: 10.1093/carcin/bgae020

Xin Yang, Limei Cui, Zhonglu Liu, Yumei Li, Xinxin Wu, Ruxian Tian, Chuanliang Jia, Chao Ren, Yakui Mou, Xicheng Song

{"title":"TMEM16A inhibits autophagy and promotes the invasion of hypopharyngeal squamous cell carcinoma through mTOR pathway.","authors":"Xin Yang, Limei Cui, Zhonglu Liu, Yumei Li, Xinxin Wu, Ruxian Tian, Chuanliang Jia, Chao Ren, Yakui Mou, Xicheng Song","doi":"10.1093/carcin/bgae020","DOIUrl":"10.1093/carcin/bgae020","url":null,"abstract":"Previous studies have indicated that transmembrane protein 16A (TMEM16A) plays a crucial role in the pathogenesis and progression of various tumors by influencing multiple signaling pathways. However, the role of TMEM16A in regulating autophagy via the mammalian target of rapamycin (mTOR) pathway and its impact on the development of hypopharyngeal squamous cell carcinoma (HSCC) remain unclear. Immunohistochemistry and western blotting were used to assess the expression of TMEM16A in HSCC tissues and metastatic lymph nodes. Manipulation of TMEM16A expression levels was achieved in the FaDu cell line through overexpression or knockdown, followed by assessment of its biological effects using cell colony formation, wound healing, transwell and invasion assays. Additionally, apoptosis and autophagy-related proteins, as well as autophagosome formation, were evaluated through western blotting, transmission electron microscopy and immunofluorescence following TMEM16A knockdown or overexpression in FaDu cells. Our study revealed significantly elevated levels of TMEM16A in both HSCC tissues and metastatic lymph nodes compared with normal tissues. In vitro experiments demonstrated that silencing TMEM16A led to a notable suppression of HSCC cell proliferation, invasion and migration. Furthermore, TMEM16A silencing effectively inhibited tumor growth in xenografted mice. Subsequent investigations indicated that knockdown of TMEM16A in HSCC cells could suppress mTOR activation, thereby triggering autophagic cell death by upregulating sequestosome-1 (SQSTM1/P62) and microtubule-associated protein light chain 3 II (LC3II). This study highlights the crucial role of TMEM16A in modulating autophagy in HSCC, suggesting its potential as a therapeutic target for the treatment of this malignancy.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":"569-581"},"PeriodicalIF":3.3,"publicationDate":"2024-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140101076","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Capsaicin enhances cisplatin-induced anti-metastasis of nasopharyngeal carcinoma by inhibiting EMT and ERK signaling via serpin family B member 2. 辣椒素通过SERPINB2抑制EMT和ERK信号转导，增强顺铂诱导的鼻咽癌抗转移能力

IF 3.3 3区医学

Carcinogenesis Pub Date : 2024-08-12 DOI: 10.1093/carcin/bgae032

Yafei Xu, Weimiao Kong, Simin Zhao, Dan Xiong, Yejun Wang

{"title":"Capsaicin enhances cisplatin-induced anti-metastasis of nasopharyngeal carcinoma by inhibiting EMT and ERK signaling via serpin family B member 2.","authors":"Yafei Xu, Weimiao Kong, Simin Zhao, Dan Xiong, Yejun Wang","doi":"10.1093/carcin/bgae032","DOIUrl":"10.1093/carcin/bgae032","url":null,"abstract":"Cisplatin (DDP)-based combined chemotherapy or concurrent chemoradiotherapy is the mainstay treatment for advanced-stage nasopharyngeal carcinoma (NPC), but needs improvement due to its severe side effects. Capsaicin (CAP) can enhance the anti-tumor activity of cytotoxic drugs. The aim of this study was to investigate the anti-metastasis activity of CAP in combination with DDP in NPC. Herein, CAP and DDP showed synergistic cytotoxic effects on NPC cells. CAP alone and DDP alone inhibited NPC migration and invasion in vitro and in vivo, and the combination of CAP and DDP had the greatest effect. Moreover, CAP upregulated the mRNA and protein expressions of serpin family B member 2 (SERPINB2). Further results showed that both SERPINB2 mRNA and protein expressions were downregulated in NPC cell lines and tissues and SERPINB2 overexpression inhibited NPC migration and invasion in vitro and in vivo, while silencing SERPINB2 acted oppositely. In addition, SERPINB2 was abnormally expressed in head and neck squamous cell carcinoma and other multiple cancers, and downregulation of SERPINB2 predicted poor prognosis in head and neck squamous cell carcinoma according to the Cancer Genome Atlas database. We further found that SERPINB2 overexpression inhibited epithelial-mesenchymal transition (EMT) and the phosphorylated extracellular signal-regulated kinase (p-ERK), and the inhibitory effect was enhanced by CAP and DDP. Altogether, our results suggest that the combined inhibition of CAP and DDP on NPC metastasis may be related to the inhibition of epithelial-mesenchymal transition and ERK signals mediated by SERPINB2, and CAP may help to improve the efficacy of DDP in the treatment of NPC and develop new therapeutic approaches.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":"556-568"},"PeriodicalIF":3.3,"publicationDate":"2024-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140956524","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Efficacy of depatuxizumab mafodotin (ABT-414) in preclinical models of head and neck cancer. 德帕妥珠单抗马福多汀（ABT-414）在头颈癌临床前模型中的疗效。

IF 3.3 3区医学

Carcinogenesis Pub Date : 2024-07-08 DOI: 10.1093/carcin/bgae014

Lucas Mani, Abdullah Naveed, Ashtyn McAdoo, Eben Rosenthal, Marisa Hom

{"title":"Efficacy of depatuxizumab mafodotin (ABT-414) in preclinical models of head and neck cancer.","authors":"Lucas Mani, Abdullah Naveed, Ashtyn McAdoo, Eben Rosenthal, Marisa Hom","doi":"10.1093/carcin/bgae014","DOIUrl":"10.1093/carcin/bgae014","url":null,"abstract":"Epidermal growth factor receptor (EGFR) is highly expressed in 80-90% of head and neck squamous cell carcinomas (HNSCCs), making it an ideal target for antibody-drug conjugates. Depatuxizumab mafodotin (ABT-414), is an EGFR-targeting ADC comprised of the monoclonal antibody ABT-806 conjugated to monomethyl auristatin F, a tubulin polymerization inhibitor. This study assessed the in vivo efficacy of ABT-414 in HNSCC. The effects of ABT-414 on HNSCCs were determined using in vitro cytotoxicity assays and in vivo flank xenograft mouse models. The distribution of ABT-414 was assessed ex vivo via optical imaging methods using a conjugate of ABT-414 to the near-infrared agent IRDye800. In vitro treatment of high EGFR-expressing human HNSCC cell lines (UMSCC47 and FaDu) with ABT-414 (0-3.38 nM) resulted in dose-dependent cell death (IC50 values of 0.213 nM and 0.167 nM, respectively). ABT-414 treatment of the FaDu mouse xenografts displayed antitumor activity (P = 0.023) without a change in body mass (P = 0.1335), whereas treatment of UMSCC47 did not generate a significant response (P = 0.1761). Fluorescence imaging revealed ABT-414-IRDye800 accumulation in the tumors of both FaDu and UMSCC47 cell lines, with a signal-to-background ratio of >10. ABT-414 treatment yielded antitumor activity in FaDu tumors, but not in UMSCC47, highlighting the potential for ABT-414 efficacy in high EGFR-expressing tumors. Although ABT-414-IRDye800 localized tumors in both cell lines, the differing antitumor responses highlight the need for further investigation into the role of the tumor microenvironment in drug delivery.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":"520-526"},"PeriodicalIF":3.3,"publicationDate":"2024-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139905081","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Long non-coding RNA KB-1460A1.5 promotes ferroptosis by inhibiting mTOR/SREBP-1/SCD1-mediated polyunsaturated fatty acid desaturation in glioma. 长非编码RNA KB-1460A1.5通过抑制胶质瘤中mTOR/SREBP-1/SCD1介导的多不饱和脂肪酸脱饱和来促进铁变态反应。

IF 3.3 3区医学

Carcinogenesis Pub Date : 2024-07-08 DOI: 10.1093/carcin/bgae016

Lixia Xu, Binli Wen, Qiaoli Wu, Shan Lu, Jianwen Liao, Lidong Mo, Qingguo Li, Xiaoguang Tong, Hua Yan

{"title":"Long non-coding RNA KB-1460A1.5 promotes ferroptosis by inhibiting mTOR/SREBP-1/SCD1-mediated polyunsaturated fatty acid desaturation in glioma.","authors":"Lixia Xu, Binli Wen, Qiaoli Wu, Shan Lu, Jianwen Liao, Lidong Mo, Qingguo Li, Xiaoguang Tong, Hua Yan","doi":"10.1093/carcin/bgae016","DOIUrl":"10.1093/carcin/bgae016","url":null,"abstract":"Ferroptosis is a new form of regulated cell death caused by the iron-dependent peroxidation of phospholipids and is related to cell metabolism, redox homeostasis and various signalling pathways related to cancer. The long non-coding RNA (lncRNA) KB-1460A1.5 acts as a tumour suppressor gene to regulate tumour growth in gliomas, but its molecular network regulatory mechanism is still unclear. In this study, we found that KB-1460A1.5 can induce ferroptosis in glioma and enhance sensitivity to RSL3, a ferroptosis inducer. Tandem mass tag proteomics and nontargeted metabolomics suggest that KB-1460A1.5 affects polyunsaturated fatty acid metabolic processes. Gas chromatography-mass spectrometry-based medium- and long-chain fatty acid-targeted metabolomics confirmed that upregulation of KB-1460A1.5 decreased the levels of monounsaturated fatty acids, oleic acid (OA) and palmitoleic acid (PO) in glioma cells. The addition of OA and PO restored KB-1460A1.5-induced cellular ferroptosis. Molecularly, KB-1460A1.5 inhibited the mammalian target of rapamycin signalling pathway to suppress the expression of downstream sterol regulatory element-binding protein 1 (SREBP-1), thereby attenuating the stearoyl-CoA desaturase-1 (SCD1)-mediated desaturation of polyunsaturated fatty acids. Finally, an animal model of subcutaneous glioma confirmed that KB-1460A1.5 could inhibit tumour progression, SREBP-1/SCD1 expression and ferroptosis. In conclusion, increasing the expression level of KB-1460A1.5 in glioma can promote the induction of oxidative stress and ferroptosis in cancer cells through SREBP-1/SCD1-mediated adipogenesis, demonstrating therapeutic potential in preclinical models.","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":"487-499"},"PeriodicalIF":3.3,"publicationDate":"2024-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139995720","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

CYR61 confers chemoresistance by upregulating survivin expression in triple-negative breast cancer. CYR61通过上调三阴性乳腺癌中存活素的表达而产生化疗耐药性。

IF 3.3 3区医学

Carcinogenesis Pub Date : 2024-07-08 DOI: 10.1093/carcin/bgae013

Hyungjoo Kim, Seogho Son, Yunhyo Ko, Hogeun Lim, Joohyung Lee, Kyung-Min Lee, Incheol Shin

引用次数: 0