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METTL5 stabilizes c-Myc by facilitating USP5 translation to reprogram glucose metabolism and promote hepatocellular carcinoma progression

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Cancer Communications 2023年第3期43卷 338-364页

作者： Peng Xia Hao Zhang Haofeng Lu Kequan Xu Xiang Jiang Yuke Jiang xiangdong gongye Zhang Chen Jie Liu Xi Chen Weijie Ma Zhonglin Zhang Yufeng Yuan Department of Hepatobiliary&Pancreatic Surgery Zhongnan Hospital ofWuhan UniversityWuhanHubeiP.R.China Clinical Medicine Research Center for Minimally Invasive Procedure of Hepatobiliary&Pancreatic Diseases of Hubei Province WuhanHubeiP.R.China Department of Hepatobiliary Surgery The First Affiliated Hospital of Yangtze UniversityJingzhouHubeiP.R.China Department of Clinical and Translational Research Center Shenzhen People’s Hospital(The Second Clinical Medical CollegeJinan UniversityThe First Affiliated HospitalSouthern University of Science and Technology)ShenzhenGuangdongP.R.China

Background:Hepatocellular carcinoma(HCC)is one of the most prevalent cancers in the world,with a high likelihood of metastasis and a dismal prognosis.The reprogramming of glucosemetabolism is critical in the development ofHCC.TheWarburg effect has recently been confirmed to occur in a variety of cancers,including HCC.However,little is known about the molecular biological mechanisms underlying the Warburg effect in HCC cells.In this study,we sought to better understand how methyltransferase 5,N6-adenosine(METTL5)controls the development of HCC and theWarburg effect.Methods:In the current study,quantitative real-time polymerase chain reaction and Western blotting were used to detect the expression of METTL5 in HCC tissues and cell lines.Several different cell models and animal models were established to determine the role of METTL5 in glucose metabolism reprogramming and the underlying molecularmechanism of HCC.Glutathione-S-transferase pulldown,coimmunoprecipitation,RNA sequencing,non-targeted metabolomics,polysome profiling,and luciferase reporter assays were performed to investigate the molecular mechanisms of METTL5 in HCC cells.Results:We discovered that METTL5 drove glucose metabolic reprogramming to promote the proliferation and metastasis of HCC.Mechanistically,upregulation of METTL5 promoted c-Myc stability and thus activated its downstream glycolytic genes lactate dehydrogenase A(LDHA),enolase 1(ENO1),triosephosphate isomerase 1(TPI1),solute carrier family 2 member 1(SLC2A1),and pyruvate kinase M2(PKM2).The c-Box and ubiquitin binding domain(UBA)regions of ubiquitin specific peptidase 5(USP5)binded to c-Myc protein and inhibited K48-linked polyubiquitination of c-Myc.Further study revealed that METTL5 controled the USP5 translation process,which in turn regulated the ubiquitination of c-Myc.Furthermore,we identified cAMP responsive element binding protein 1(CREB1)/P300 as a critical transcriptional regulator ofMETTL5 that promoted the transcription of METTL5 in HCC.In patient-derived tumor xenograft(PDX)m

关键词： METTL5 c-Myc USP5 P300 CREB1 deubiquitination hepatocellular carcinoma glucose metabolism

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Research progress on immunotherapy targeting the tumor immune microenvironment for cholangiocarcinoma

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Oncology and Translational Medicine 2023年第2期9卷 49-55页

作者： Tianyin Ma Zhang Chen Yibo Chai xiangdong gongye Peng Xia Chenming Qu Ming Tian Yufeng Yuan Department of Hepatobiliary and Pancreatic Surgery Zhongnan Hospital of Wuhan UniversityWuhan 430071China Clinical Medicine Research Center for Minimally Invasive Procedure of Hepatobiliary&Pancreatic Diseases of Hubei Province Wuhan 430071China TaiKang Center for Life and Medical Sciences Wuhan UniversityWuhan 430071China

Cholangiocarcinoma(CCA)is the second most common hepatobiliary cancer,and its incidence has increased significantly in recent years.CCA has poor prognosis owing to the limited diagnosis and treatment options.The tumor immune microenvironment(TIME),which comprises immune cells,cytokines,and chemokines,plays a significant role in cancer progression,the evasion of immune surveillance,and therapeutic responses.Immunotherapeutic strategies targeting the TIME offer the potential for the recognition and eradication of CCA.This review discusses the cellular and molecular components of the TIME in CCA and immunotherapeutic strategies targeting it.

关键词： diagnosis immune cancer

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