Molecular Cancer Research最新文献_第8页

Expanding Our Horizon to Inform Cutting Edge Mechanistic Studies: Cancer Research Resources. 扩大我们的视野，为前沿机制研究提供信息：癌症研究资源。

IF 4.1 2区医学

Molecular Cancer Research Pub Date : 2024-11-01 DOI: 10.1158/1541-7786.MCR-24-0884

Massimo Loda

引用次数: 0

METTL14-Mediated Bim mRNA m6A Modification Augments Osimertinib Sensitivity in EGFR-Mutant NSCLC Cells. METTL14 介导的 Bim mRNA m6A 修饰增强了表皮生长因子受体突变 NSCLC 细胞对奥希替尼的敏感性。

IF 4.1 2区医学

Molecular Cancer Research Pub Date : 2024-11-01 DOI: 10.1158/1541-7786.MCR-23-1018

Siwen Fan, Xinwu Lv, Chuantao Zhang, Bingbing Zeng, Yanqing Liang, Danyang Chen, Zumin Xu, Pan Li, Shanshan Wu, Hao Liu, Kai Luo, Zongcai Liu, Yanmei Yi

{"title":"METTL14-Mediated Bim mRNA m6A Modification Augments Osimertinib Sensitivity in EGFR-Mutant NSCLC Cells.","authors":"Siwen Fan, Xinwu Lv, Chuantao Zhang, Bingbing Zeng, Yanqing Liang, Danyang Chen, Zumin Xu, Pan Li, Shanshan Wu, Hao Liu, Kai Luo, Zongcai Liu, Yanmei Yi","doi":"10.1158/1541-7786.MCR-23-1018","DOIUrl":"10.1158/1541-7786.MCR-23-1018","url":null,"abstract":"Resistance to osimertinib represents a significant challenge for the successful treatment of non-small cell lung cancer (NSCLC) harboring activating mutations in EGFR. N6-methyladenosine (m6A) on mRNAs is critical for various biological processes, yet whether m6A regulates osimertinib resistance of NSCLC remains unknown. In this study, we demonstrated that developing osimertinib-resistant phenotypes depends on m6A reduction resulting from downexpression of m6A methyltransferase METTL14 in EGFR-mutant NSCLCs. Both in vitro and in vivo assays showed that specific knockdown of METTL14 was sufficient to confer osimertinib resistance and that elevated expression of METTL14 rescued the efficacy of osimertinib in the resistant NSCLC cells. Mechanistically, METTL14 promoted m6A methylation of pro-apoptotic Bim mRNA and increased Bim mRNA stability and expression, resulting in activating the Bim-dependent pro-apoptotic signaling and thereby promoting osimertinib-induced cell apoptosis. Analysis of clinical samples revealed that decreased expression of METTL14 was observed in osimertinib-resistant NSCLC tissues and significantly associated with a poor prognosis. In conclusion, our study reveals a novel regulatory mechanism by which METTL14-mediated m6A methylation of Bim mRNA inhibited osimertinib resistance of NSCLC cells. It offers more evidences for the involvement of m6A modification in regulation of osimertinib resistance and provides potential therapeutic targets for novel approaches to overcome the tolerance of osimertinib and other EGFR tyrosine kinase inhibitors. Implications: This study offers more evidences for the involvement of METTL14-mediated N6-methyladenosine modification in regulation of osimertinib resistance and provides potential therapeutic targets for novel approaches to overcome the tolerance of osimertinib and other EGFR tyrosine kinase inhibitors.","PeriodicalId":19095,"journal":{"name":"Molecular Cancer Research","volume":" ","pages":"1051-1063"},"PeriodicalIF":4.1,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141492786","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}

引用次数: 0

Retraction: KRAS Activation in Gastric Adenocarcinoma Stimulates Epithelial-to-Mesenchymal Transition to Cancer Stem-Like Cells and Promotes Metastasis. 撤回：胃腺癌中的 KRAS 激活会刺激上皮细胞向癌干样细胞的间质转化并促进转移。

IF 4.1 2区医学

Molecular Cancer Research Pub Date : 2024-11-01 DOI: 10.1158/1541-7786.MCR-24-0858

Changhwan Yoon, Jacob Till, Soo-Jeong Cho, Kevin K Chang, Jian-Xian Lin, Chang-Ming Huang, Sandra Ryeom, Sam S Yoon

引用次数: 0

NAP1L1 Promotes Endometrial Cancer Progression via EP300-Mediated DDX5 Promoter Acetylation. NAP1L1 通过 EP300 介导的 DDX5 启动子乙酰化促进子宫内膜癌进展

IF 4.1 2区医学

Molecular Cancer Research Pub Date : 2024-11-01 DOI: 10.1158/1541-7786.MCR-23-0871

Xiangfei Zhu, Yishan Li, Zhiying Shao, Xiaoyuan Lu, Youguo Chen

{"title":"NAP1L1 Promotes Endometrial Cancer Progression via EP300-Mediated DDX5 Promoter Acetylation.","authors":"Xiangfei Zhu, Yishan Li, Zhiying Shao, Xiaoyuan Lu, Youguo Chen","doi":"10.1158/1541-7786.MCR-23-0871","DOIUrl":"10.1158/1541-7786.MCR-23-0871","url":null,"abstract":"Endometrial cancer is one of the predominant tumors of the female reproductive system. In this current study, we investigated the functions and related mechanisms of nucleosome assembly protein 1 like 1 (NAP1L1)/ DEAD-box helicase 5 (DDX5) in endometrial cancer. This retrospective study analyzed the medical records of patients with endometrial cancer, collected tissue samples for NAP1L1 and DDX5 staining, and conducted survival analysis using the Kaplan-Meier method. To evaluate the impact of NAP1L1 and/or DDX5 on cellular processes in endometrial cancer cells, several techniques were employed. These included Cell Counting Kit-8 assay, wound healing assay, Transwell assay, as well as overexpression or knockdown of target gene expression. Additionally, chromatin immunoprecipitation, dual luciferase reporter gene, and coimmunoprecipitation (Co-IP) assay were utilized to confirm the interaction between NAP1L1, E1A-binding protein p300 (EP300), and DDX5. Furthermore, qRT-PCR, Western blot, and Co-IP assay were performed to analyze the modulation of NAP1L1/DDX5 in Wnt/β-catenin. NAP1L1 and DDX5 expression were upregulated in endometrial cancer tissues, and correlated with poor prognosis. NAP1L1/DDX5 promoted endometrial cancer cell proliferation, migration, and invasion. NAP1L1 promotes acetylation and transcription by recruiting EP300 to the DDX5 promoter. DDX5 could activate Wnt/β-catenin signal by binding to β-catenin. In animal models, knockdown of NAP1L1 inhibits endometrial cancer tumor growth and lung metastasis. To sum up, our study demonstrated that NAP1L1 promoted the malignant phenotypes of endometrial cancer cells via recruiting EP300 to promote DDX5 acetylation, thus activating the Wnt/β-catenin signaling pathway. Implications: Our research findings indicate that targeting the NAP1L1/EP300/DX5 axis might be a new potential treatment option for endometrial cancer.","PeriodicalId":19095,"journal":{"name":"Molecular Cancer Research","volume":" ","pages":"1011-1021"},"PeriodicalIF":4.1,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141492801","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}

引用次数: 0

lncRNA-WAL Promotes Triple-Negative Breast Cancer Aggression by Inducing β-Catenin Nuclear Translocation. lncRNA-WAL通过诱导β-catenin核易位促进三阴性乳腺癌的侵袭。

IF 4.1 2区医学

Molecular Cancer Research Pub Date : 2024-11-01 DOI: 10.1158/1541-7786.MCR-23-0334

Hongyan Huang, Haiyun Jin, Rong Lei, Zhanghai He, Shishi He, Jiewen Chen, Phei E Saw, Zhu Qiu, Guosheng Ren, Yan Nie

{"title":"lncRNA-WAL Promotes Triple-Negative Breast Cancer Aggression by Inducing β-Catenin Nuclear Translocation.","authors":"Hongyan Huang, Haiyun Jin, Rong Lei, Zhanghai He, Shishi He, Jiewen Chen, Phei E Saw, Zhu Qiu, Guosheng Ren, Yan Nie","doi":"10.1158/1541-7786.MCR-23-0334","DOIUrl":"10.1158/1541-7786.MCR-23-0334","url":null,"abstract":"Because of its insensitivity to existing radiotherapy, namely, chemotherapy and targeted treatments, triple-negative breast cancer (TNBC) remains a great challenge to overcome. Increasing evidence has indicated abnormal Wnt/β-catenin pathway activation in TNBC but not luminal or HER2+ breast cancer, and lncRNAs play a key role in a variety of cancers. Through lncRNA microarray profiling between activated and inactivated Wnt/β-catenin pathway of TNBC tissues, lnc-WAL (Wnt/β-catenin-associated lncRNA; WAL) was selected as the top upregulated lncRNA in Wnt/β-catenin pathway activation compared with the inactivation group. RNA immunoprecipitation sequencing was used to compare the β-catenin and IgG groups, in which lnc-WAL could interact with β-catenin. Clinically, increased lnc-WAL in TNBC tumor tissue was associated with shorter survival. lnc-WAL promoted epithelial-mesenchymal transition, the proliferation, migration, and invasion of breast cancer stem cells and TNBC cells. Mechanistically, lnc-WAL inhibited β-catenin protein degradation via AXIN-mediated phosphorylation at serine 45. Subsequently, β-catenin accumulated in the nucleus and activated the target genes. Importantly, Wnt/β-catenin pathway activation stimulated the transcription of lnc-WAL. These results pointed to a master regulatory role of lnc-WAL/AXIN/β-catenin in the malignant progression of TNBC. Our findings provide important clinical translational evidence that lnc-WAL may be a potential therapeutic target against TNBC. Implications: The positive feedback between lnc-WAL and the Wnt/β-catenin pathway promotes TNBC progression, and lnc-WAL could be a potential prognostic marker for patients with TNBC.","PeriodicalId":19095,"journal":{"name":"Molecular Cancer Research","volume":" ","pages":"1036-1050"},"PeriodicalIF":4.1,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11528204/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141469682","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}

引用次数: 0

hnRNPAB Promotes Pancreatic Ductal Adenocarcinoma Extravasation and Liver Metastasis by Stabilizing MYC mRNA. HnRNPAB 通过稳定 MYC mRNA 促进胰腺导管腺癌的外渗和肝转移。

IF 4.1 2区医学

Molecular Cancer Research Pub Date : 2024-11-01 DOI: 10.1158/1541-7786.MCR-24-0110

Ke Lei, Mingyue Sun, Xianghan Chen, Jia Wang, Xiaolan Liu, Ying Ning, Shuai Ping, Ruining Gong, Yu Zhang, Gong Qing, Chenyang Zhao, He Ren

{"title":"hnRNPAB Promotes Pancreatic Ductal Adenocarcinoma Extravasation and Liver Metastasis by Stabilizing MYC mRNA.","authors":"Ke Lei, Mingyue Sun, Xianghan Chen, Jia Wang, Xiaolan Liu, Ying Ning, Shuai Ping, Ruining Gong, Yu Zhang, Gong Qing, Chenyang Zhao, He Ren","doi":"10.1158/1541-7786.MCR-24-0110","DOIUrl":"10.1158/1541-7786.MCR-24-0110","url":null,"abstract":"Heterogeneous nuclear ribonucleoprotein AB (hnRNPAB) is considered a cancer-promoting heterogeneous nuclear ribonucleoprotein in many cancers, but its function in pancreatic ductal adenocarcinoma (PDAC) is poorly understood. hnRNPAB was highly expressed in PDAC tissues compared with normal pancreatic tissues, and high expression of hnRNPAB was associated with poor overall survival and recurrence-free survival in patients with PDAC. hnRNPAB promotes migration and invasion of PDAC cells in vitro. In xenograft tumor mouse models, hnRNPAB deprivation significantly attenuated liver metastasis. hnRNPAB mRNA and protein levels are positively associated with MYC in PDAC cells. Mechanistically, hnRNPAB bound to MYC mRNA and prolonged its half-life. hnRNPAB induced PDAC cells to secrete CXCL8 via MYC, which promoted neutrophil recruitment and facilitated tumor cells entrancing into the hepatic parenchyma. These findings point to a novel regulatory mechanism via which hnRNPAB promotes PDAC metastasis. Implications: hnRNPAB participates in the posttranscriptional regulation of the oncogene MYC by binding and stabilizing MYC mRNA, thereby promoting liver metastasis in PDAC.","PeriodicalId":19095,"journal":{"name":"Molecular Cancer Research","volume":" ","pages":"1022-1035"},"PeriodicalIF":4.1,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141534886","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}

引用次数: 0

Ubiquitin Ligase TRIM22 Inhibits Ovarian Cancer Malignancy via TCF4 Degradation. 泛素连接酶TRIM22通过TCF4降解抑制卵巢癌恶变

IF 4.1 2区医学

Molecular Cancer Research Pub Date : 2024-10-02 DOI: 10.1158/1541-7786.MCR-23-0962

Tao Tao, Yongqi Zhang, Chunyan Guan, Shuxiang Wang, Xiaoli Liu, Min Wang

{"title":"Ubiquitin Ligase TRIM22 Inhibits Ovarian Cancer Malignancy via TCF4 Degradation.","authors":"Tao Tao, Yongqi Zhang, Chunyan Guan, Shuxiang Wang, Xiaoli Liu, Min Wang","doi":"10.1158/1541-7786.MCR-23-0962","DOIUrl":"10.1158/1541-7786.MCR-23-0962","url":null,"abstract":"Ovarian cancer is one of the most common malignancies in women. Tripartite motif-containing protein 22 (TRIM22) plays an important role in the initiation and progression of malignant tumors. Similarly, the transcription factor 4 (TCF4) is an essential factor involved in the initiation and progression of many tumors. However, it is still unclear whether TRIM22 can affect TCF4 in ovarian cancer. Therefore, this study aims to investigate the mechanism related to TRIM22 and TCF4 in ovarian cancer. TRIM22 protein and mRNA levels were analyzed in samples from clinical and cell lines. The effects of TRIM22 knockdown and overexpression on cell proliferation, colony formation, migration, invasion, and related biomarkers were evaluated. In addition, the role of ubiquitination-mediated degradation of TCF4 was investigated by qRT-PCR and Western blotting. The association between TRIM22 and TCF4 was evaluated by Western blotting, coimmunoprecipitation, proliferation, colony formation, invasion, migration, and related biomarkers. The results showed that the expression of TRIM22 was minimal in ovarian cancer tissues. Furthermore, upregulation of TRIM22 significantly inhibited ovarian cancer cell proliferation, colony formation, migration, and invasion. In addition, TRIM22 was observed to regulate the degradation of TCF4 through the ubiquitination pathway. TCF4 can reverse the effects of TRIM22 on proliferation, colony formation, migration, and invasion in ovarian cancer cells. TRIM22-mediated ubiquitination of TCF4 at K48 is facilitated by the RING domain. Implications: In conclusion, ubiquitination of TCF4 protein in ovarian cancer is regulated by TRIM22, which has the potential to limit the proliferation, migration, and invasion of ovarian cancer.","PeriodicalId":19095,"journal":{"name":"Molecular Cancer Research","volume":" ","pages":"943-956"},"PeriodicalIF":4.1,"publicationDate":"2024-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141262339","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}

引用次数: 0

RNA-Binding Protein Lin28B Promotes Chronic Myeloid Leukemia Blast Crisis by Transcriptionally Upregulating miR-181d. RNA结合蛋白Lin28B通过转录上调miR-181d促进慢性髓性白血病爆发危象。

IF 4.1 2区医学

Molecular Cancer Research Pub Date : 2024-10-02 DOI: 10.1158/1541-7786.MCR-23-0928

Minran Zhou, Xiaolin Yin, Lu Zhang, Zelong Cui, Xinwen Jiang, Qingli Ji, Sai Ma, Chunyan Chen

{"title":"RNA-Binding Protein Lin28B Promotes Chronic Myeloid Leukemia Blast Crisis by Transcriptionally Upregulating miR-181d.","authors":"Minran Zhou, Xiaolin Yin, Lu Zhang, Zelong Cui, Xinwen Jiang, Qingli Ji, Sai Ma, Chunyan Chen","doi":"10.1158/1541-7786.MCR-23-0928","DOIUrl":"10.1158/1541-7786.MCR-23-0928","url":null,"abstract":"The blast crisis (BC) of chronic myeloid leukemia (CML) has poor efficacy against existing treatments and extremely short survival. However, the molecular mechanism of CML-chronic phase (CP) transformation to CML-BC is not yet fully understood. Here, we show that Lin28B, an RNA-binding protein, acted as an activator enhancing the transformation to CML-BC by mediating excessive cell proliferation. The level of Lin28B expression was apparently elevated in patients with CML-BC compared with newly diagnosed patients with CML-CP. The overexpression of Lin28B promoted the proliferation of leukemia cells. Mechanistically, we identified Lin28B as a DNA-binding protein by binding to the promoter region of miR-181d and upregulating its expression, which inhibited the expression of programmed cell death 4 (PDCD4) by binding to the PDCD4 3'UTR region, thereby enhancing the proliferation of CML cells. Overall, the \"Lin28B-miR-181d-PDCD4\" regulatory axis promoted CML blast crisis. Implications: Our findings highlight the oncogenic role of Lin28B in CML blast crisis, acting as a DNA-binding protein that transcriptionally upregulates miR-181d expression.","PeriodicalId":19095,"journal":{"name":"Molecular Cancer Research","volume":" ","pages":"932-942"},"PeriodicalIF":4.1,"publicationDate":"2024-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141284297","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}

引用次数: 0

The Complex Regulation of Cytokinesis upon Abscission Checkpoint Activation. 脱落检查点激活时对细胞分裂的复杂调控。

IF 4.1 2区医学

Molecular Cancer Research Pub Date : 2024-10-02 DOI: 10.1158/1541-7786.MCR-24-0365

Paulius Gibieža, Vilma Petrikaitė

{"title":"The Complex Regulation of Cytokinesis upon Abscission Checkpoint Activation.","authors":"Paulius Gibieža, Vilma Petrikaitė","doi":"10.1158/1541-7786.MCR-24-0365","DOIUrl":"10.1158/1541-7786.MCR-24-0365","url":null,"abstract":"Cytokinetic abscission is a crucial process that guides the separation of daughter cells at the end of each cell division. This process involves the cleavage of the intercellular bridge, which connects the newly formed daughter cells. Over the years, researchers have identified several cellular contributors and intracellular processes that influence the spatial and temporal distribution of the cytoskeleton during cytokinetic abscission. This review presents the most important scientific discoveries that allow activation of the abscission checkpoint, ensuring a smooth and successful separation of a single cell into two cells during cell division. Here, we describe different factors, such as abscission checkpoint, ICB tension, nuclear pore defects, DNA replication stress, chromosomal stability, and midbody proteins, which play a role in the regulation and correct timing of cytokinetic abscission. Furthermore, we explore the downsides associated with the dysregulation of abscission, including its negative impact on cells and the potential to induce tumor formation in humans. Finally, we propose a novel factor for improving cancer therapy and give future perspectives in this research field.","PeriodicalId":19095,"journal":{"name":"Molecular Cancer Research","volume":" ","pages":"909-919"},"PeriodicalIF":4.1,"publicationDate":"2024-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141971526","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}

引用次数: 0

Lactate Induces Tumor Progression via LAR Motif-Dependent Yin-Yang 1 Degradation. 乳酸通过依赖于 LAR motif 的阴阳 1 降解诱导肿瘤进展。

IF 4.1 2区医学

Molecular Cancer Research Pub Date : 2024-10-02 DOI: 10.1158/1541-7786.MCR-23-0583

Shujuan Du, Xiaoting Chen, Xiao Han, Yuyan Wang, Dan Yu, Ying Li, Caixia Zhu, Yin Tong, Shujun Gao, Junwen Wang, Fang Wei, Qiliang Cai

{"title":"Lactate Induces Tumor Progression via LAR Motif-Dependent Yin-Yang 1 Degradation.","authors":"Shujuan Du, Xiaoting Chen, Xiao Han, Yuyan Wang, Dan Yu, Ying Li, Caixia Zhu, Yin Tong, Shujun Gao, Junwen Wang, Fang Wei, Qiliang Cai","doi":"10.1158/1541-7786.MCR-23-0583","DOIUrl":"10.1158/1541-7786.MCR-23-0583","url":null,"abstract":"The metabolic reprogramming of aerobic glycolysis contributes to tumorigenesis. High plasma lactate is a critical regulator in the development of many human malignancies; however, the underlying molecular mechanisms of cancer progression in response to lactate (LA) remain elusive. Here, we show that the reduction of Yin-Yang 1 (YY1) expression correlated with high LA commonly occurs in various cancer cell types, including B-lymphoma and cervical cancer. Mechanistically, LA induces YY1 nuclear export and degradation via HSP70-mediated autophagy adjacent to mitochondria in a histidine (His)-rich LA-responsive (LAR) motif-dependent manner. The mutation of the LAR motif blocks LA-mediated YY1 cytoplasmic accumulation and in turn enhances cell apoptosis. Furthermore, low expression of YY1 promotes colony formation, invasion, angiogenesis, and growth of cancer cells in response to LA in vitro and in vivo using a murine xenograft model. Taken together, our findings reveal a key LAR element and may serve as therapeutic target for intervening cancer progression. Implications: We have shown that lactate can induce YY1 degradation via its His-rich LAR motif and low expression of YY1 promotes cancer cell progression in response to lactate, leading to better prediction of YY1 targeting therapy.","PeriodicalId":19095,"journal":{"name":"Molecular Cancer Research","volume":" ","pages":"957-972"},"PeriodicalIF":4.1,"publicationDate":"2024-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141420015","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}

引用次数: 0