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133 results on '"Zhang, Chris Zhiyi"'

14. LINC00493‐encoded microprotein SMIM26 exerts anti‐metastatic activity in renal cell carcinoma.

Author

Meng, Kun, Lu, Shaohua, Li, Yu‐Ying, Hu, Li‐Ling, Zhang, Jing, Cao, Yun, Wang, Yang, Zhang, Chris Zhiyi, and He, Qing‐Yu

Abstract

Human microproteins encoded by long non‐coding RNAs (lncRNA) have been increasingly discovered, however, complete functional characterization of these emerging proteins is scattered. Here, we show that LINC00493‐encoded SMIM26, an understudied microprotein localized in mitochondria, is tendentiously downregulated in clear cell renal cell carcinoma (ccRCC) and correlated with poor overall survival. LINC00493 is recognized by RNA‐binding protein PABPC4 and transferred to ribosomes for translation of a 95‐amino‐acid protein SMIM26. SMIM26, but not LINC00493, suppresses ccRCC growth and metastatic lung colonization by interacting with acylglycerol kinase (AGK) and glutathione transport regulator SLC25A11 via its N‐terminus. This interaction increases the mitochondrial localization of AGK and subsequently inhibits AGK‐mediated AKT phosphorylation. Moreover, the formation of the SMIM26‐AGK‐SCL25A11 complex maintains mitochondrial glutathione import and respiratory efficiency, which is abrogated by AGK overexpression or SLC25A11 knockdown. This study functionally characterizes the LINC00493‐encoded microprotein SMIM26 and establishes its anti‐metastatic role in ccRCC, and therefore illuminates the importance of hidden proteins in human cancers. Synopsis: LINC00493‐derived mitochondrial microprotein SMIM26 suppresses clear cell renal cell carcinoma metastasis via interaction with AGK and SLC25A11 to inactivate AKT signaling. SMIM26 is a microprotein encoded by LINC00493 and localizes to mitochondria.Translation of SMIM26 is mediated by the RNA‐binding protein PABPC4.SMIM26 interacts with acylglycerol kinase (AGK) and glutathione transport regulator SLC25A11.The tripartite complex of SMIM26‐AGK‐SLC25A11 maintains mitochondrial homeostasis and suppresses ccRCC metastasis. [ABSTRACT FROM AUTHOR]

Published
2023
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28. Role of Porcine Fibrin Sealant in the Prevention of Cervical Anastomotic Leakage After Esophagectomy for Esophageal or Esophagogastric Junction Cancer (PLACE020): A Phase 2, Single-Arm, Prospective Study

Author

Lin, Yaobin, primary, Hu, Yihuai, additional, Huang, Yan, additional, Luo, Kongjia, additional, Wang, Kexi, additional, Bella, Amos Éla, additional, Lai, Rencun, additional, Li, Yi, additional, Situ, Dongrong, additional, Wu, Shuyun, additional, Chen, Jiyang, additional, Lin, Ting, additional, D’Journo, Xavier Benoit, additional, Novoa, Nuria M., additional, Brunelli, Alessandro, additional, Fernando, Hiran C., additional, Cerfolio, Robert J., additional, Ismail, Mahmoud, additional, Zhang, Chris Zhiyi, additional, Fu, Jianhua, additional, Yang, Hong, additional, and Group, AME Thoracic Surgery Collaborative, additional

Published
2019
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29. A Coiled‐Coil Domain Containing 50 Splice Variant Is Modulated by Serine/Arginine‐Rich Splicing Factor 3 and Promotes Hepatocellular Carcinoma in Mice by the Ras Signaling Pathway

Author

Wang, Hong, primary, Zhang, Chris Zhiyi, additional, Lu, Shi‐Xun, additional, Zhang, Mei‐Fang, additional, Liu, Li‐Li, additional, Luo, Rong‐Zhen, additional, Yang, Xia, additional, Wang, Chun‐Hua, additional, Chen, Shi‐Lu, additional, He, Yang‐Fan, additional, Xie, Dan, additional, Xu, Rui‐Hua, additional, and Yun, Jing‐Ping, additional

Published
2018
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40. TRIM65 triggers β-catenin signaling via ubiquitylation of Axin1 to promote hepatocellular carcinoma.

Author

Yu-Feng Yang, Mei-Fang Zhang, Qiu-Hong Tian, and Zhang, Chris Zhiyi

Subjects
UBIQUITIN ligases, CANCER invasiveness, LIVER cancer
Abstract

Deregulation of ubiquitin ligases contributes to the malignant progression of human cancers. Tripartite motif-containing protein 65 (TRIM65) is an E3 ubiquitin ligase and has been implicated in human diseases, but its role and clinical significance in hepatocellular carcinoma (HCC) remain unknown. Here, we showed that TRIM65 expression was increased in HCC tissues and associated with poor outcome in two independent cohorts containing 888 patients. In vitro and in vivo data demonstrated that overexpression of TRIM65 promoted cell growth and tumor metastasis, whereas knockdown of TRIM65 resulted in opposite phenotypes. Further studies revealed that TRIM65 exerted oncogenic activities via ubiquitylation of Axin1 to activate the β-catenin signaling pathway. TRIM65 directly bound to Axin1 and accelerated its degradation through ubiquitylation. Furthermore, HMGA1 was identified as an upstream regulator of TRIM65 in HCC cells. In clinical samples, TRIM65 expression was positively correlated with the expression of HMGA1 and nuclear β-catenin. Collectively, our data indicate that TRIM65 functions as an oncogene in HCC. The newly identified HMGA1/TRIM65/β-catenin axis serves as a promising prognostic factor and therapeutic target. [ABSTRACT FROM AUTHOR]

Published
2017
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50. HnRNPR-mediated UPF3B mRNA splicing drives hepatocellular carcinoma metastasis.

Author

Wang H, Qian D, Wang J, Liu Y, Luo W, Zhang H, Cheng J, Li H, Wu Y, Li W, Wang J, Yang X, Zhang T, Han D, Wang Q, Zhang CZ, and Liu L

Abstract

Introduction: Abnormal alternative splicing (AS) contributes to aggressive intrahepatic invasion and metastatic spread, leading to the high lethality of hepatocellular carcinoma (HCC)., Objectives: This study aims to investigate the functional implications of UPF3B-S (a truncated oncogenic splice variant) in HCC metastasis., Methods: Basescope assay was performed to analyze the expression of UPF3B-S mRNA in tissues and cells. RNA immunoprecipitation, and in vitro and in vivo models were used to explore the role of UPF3B-S and the underlying mechanisms., Results: We show that splicing factor HnRNPR binds to the pre-mRNA of UPF3B via its RRM2 domain to generate an exon 8 exclusion truncated splice variant UPF3B-S. High expression of UPF3B-S is correlated with tumor metastasis and unfavorable overall survival in patients with HCC. The knockdown of UPF3B-S markedly suppresses the invasive and migratory capacities of HCC cells in vitro and in vivo. Mechanistically, UPF3B-S protein targets the 3'-UTR of CDH1 mRNA to enhance the degradation of CDH1 mRNA, which results in the downregulation of E-cadherin and the activation of epithelial-mesenchymal transition. Overexpression of UPF3B-S enhances the dephosphorylation of LATS1 and the nuclear accumulation of YAP1 to trigger the Hippo signaling pathway., Conclusion: Our findings suggest that HnRNPR-induced UPF3B-S promotes HCC invasion and metastasis by exhausting CDH1 mRNA and modulating YAP1-Hippo signaling. UPF3B-S could potentially serve as a promising biomarker for the clinical management of invasive HCC., (Copyright © 2023. Production and hosting by Elsevier B.V.)

Published
2024
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