Knockdown of ZNF479 inhibits proliferation and glycolysis of gastric cancer cells through regulating β‐catenin/c‐Myc signaling pathway

Abstract Gastric cancer is the fifth most common malignancy and the third most deadly tumor in the world. Zinc finger protein 479 (ZNF479) has been demonstrated to play crucial roles in hepatocellular carcinoma. However, the function of ZNF479 in gastric cancer remains to be clarified. The current s...

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Main Authors: Xiao‐Sheng Jin, Ting‐Ting Ji, Zheng‐Chao Shi, Qing‐Qing Zhang, Fang‐Peng Ye, Wei‐Lai Yu, Rong‐Zhou Li
Format: Article
Language:English
Published: Wiley 2021-09-01
Series:Kaohsiung Journal of Medical Sciences
Subjects:
Online Access:https://doi.org/10.1002/kjm2.12399
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author Xiao‐Sheng Jin
Ting‐Ting Ji
Zheng‐Chao Shi
Qing‐Qing Zhang
Fang‐Peng Ye
Wei‐Lai Yu
Rong‐Zhou Li
author_facet Xiao‐Sheng Jin
Ting‐Ting Ji
Zheng‐Chao Shi
Qing‐Qing Zhang
Fang‐Peng Ye
Wei‐Lai Yu
Rong‐Zhou Li
author_sort Xiao‐Sheng Jin
collection DOAJ
description Abstract Gastric cancer is the fifth most common malignancy and the third most deadly tumor in the world. Zinc finger protein 479 (ZNF479) has been demonstrated to play crucial roles in hepatocellular carcinoma. However, the function of ZNF479 in gastric cancer remains to be clarified. The current study aimed to investigate the role of ZNF479 in gastric cancer progression and elucidate the potential molecular mechanism. In this study, Cell Count Kit‐8 and colony formation assays demonstrated that knockdown of ZNF479 inhibited cell proliferation in AGS and SGC‐7901 cells. Of note, knockdown of ZNF479 hinders tumor growth of xenograft tumor mice. What is more, knockdown of ZNF479 inhibited glucose uptake, lactate production, adenosine triphosphate level, and extracellular acidification ratio; increased oxygen consumption ratio in gastric cancer cells; and decreased the expression of glycolytic proteins both in vitro and in vivo. Furthermore, analysis mechanism suggests that ZNF479 participated in the regulation of gastric cancer progression through affecting the β‐catenin/c‐Myc signaling pathway. Collectively, ZNF479 plays a role as an oncogene through modulating β‐catenin/c‐Myc signaling pathway in the development of gastric cancer, which provides a new research target for future studies.
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spelling doaj.art-6ef02df05cde4653af5e0b0afadd612c2022-12-21T21:31:58ZengWileyKaohsiung Journal of Medical Sciences1607-551X2410-86502021-09-0137975976710.1002/kjm2.12399Knockdown of ZNF479 inhibits proliferation and glycolysis of gastric cancer cells through regulating β‐catenin/c‐Myc signaling pathwayXiao‐Sheng Jin0Ting‐Ting Ji1Zheng‐Chao Shi2Qing‐Qing Zhang3Fang‐Peng Ye4Wei‐Lai Yu5Rong‐Zhou Li6Department of Gastroenterology Ruian people's hospital Rui'an City ChinaDepartment of Gastroenterology Ruian people's hospital Rui'an City ChinaDepartment of Gastroenterology Ruian people's hospital Rui'an City ChinaDepartment of Gastroenterology Ruian people's hospital Rui'an City ChinaDepartment of Gastroenterology Ruian people's hospital Rui'an City ChinaDepartment of Gastroenterology Ruian people's hospital Rui'an City ChinaDepartment of Gastroenterology Ruian people's hospital Rui'an City ChinaAbstract Gastric cancer is the fifth most common malignancy and the third most deadly tumor in the world. Zinc finger protein 479 (ZNF479) has been demonstrated to play crucial roles in hepatocellular carcinoma. However, the function of ZNF479 in gastric cancer remains to be clarified. The current study aimed to investigate the role of ZNF479 in gastric cancer progression and elucidate the potential molecular mechanism. In this study, Cell Count Kit‐8 and colony formation assays demonstrated that knockdown of ZNF479 inhibited cell proliferation in AGS and SGC‐7901 cells. Of note, knockdown of ZNF479 hinders tumor growth of xenograft tumor mice. What is more, knockdown of ZNF479 inhibited glucose uptake, lactate production, adenosine triphosphate level, and extracellular acidification ratio; increased oxygen consumption ratio in gastric cancer cells; and decreased the expression of glycolytic proteins both in vitro and in vivo. Furthermore, analysis mechanism suggests that ZNF479 participated in the regulation of gastric cancer progression through affecting the β‐catenin/c‐Myc signaling pathway. Collectively, ZNF479 plays a role as an oncogene through modulating β‐catenin/c‐Myc signaling pathway in the development of gastric cancer, which provides a new research target for future studies.https://doi.org/10.1002/kjm2.12399c‐Mycgastric cancerglycolysisproliferationZNF479
spellingShingle Xiao‐Sheng Jin
Ting‐Ting Ji
Zheng‐Chao Shi
Qing‐Qing Zhang
Fang‐Peng Ye
Wei‐Lai Yu
Rong‐Zhou Li
Knockdown of ZNF479 inhibits proliferation and glycolysis of gastric cancer cells through regulating β‐catenin/c‐Myc signaling pathway
Kaohsiung Journal of Medical Sciences
c‐Myc
gastric cancer
glycolysis
proliferation
ZNF479
title Knockdown of ZNF479 inhibits proliferation and glycolysis of gastric cancer cells through regulating β‐catenin/c‐Myc signaling pathway
title_full Knockdown of ZNF479 inhibits proliferation and glycolysis of gastric cancer cells through regulating β‐catenin/c‐Myc signaling pathway
title_fullStr Knockdown of ZNF479 inhibits proliferation and glycolysis of gastric cancer cells through regulating β‐catenin/c‐Myc signaling pathway
title_full_unstemmed Knockdown of ZNF479 inhibits proliferation and glycolysis of gastric cancer cells through regulating β‐catenin/c‐Myc signaling pathway
title_short Knockdown of ZNF479 inhibits proliferation and glycolysis of gastric cancer cells through regulating β‐catenin/c‐Myc signaling pathway
title_sort knockdown of znf479 inhibits proliferation and glycolysis of gastric cancer cells through regulating β catenin c myc signaling pathway
topic c‐Myc
gastric cancer
glycolysis
proliferation
ZNF479
url https://doi.org/10.1002/kjm2.12399
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