G-protein Coupled Receptor 34 Knockdown Impairs the Proliferation and Migration of HGC-27 Gastric Cancer Cells In Vitro
Background: Overexpression of G-protein coupled receptor 34 (GPR34) affects the progression and prognosis of human gastric adenocarcinoma, however, the role of GPR34 in gastric cancer development and progression has not been well-determined. The current study aimed to investigate the effect of GPR34...
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Language: | English |
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Wolters Kluwer
2015-01-01
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Series: | Chinese Medical Journal |
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Online Access: | http://www.cmj.org/article.asp?issn=0366-6999;year=2015;volume=128;issue=4;spage=545;epage=549;aulast=Jin |
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author | Zhong-Tian Jin Kun Li Mei Li Zhi-Gang Ren Fu-Shun Wang Ji-Ye Zhu Xi-Sheng Leng Wei-Dong Yu |
author_facet | Zhong-Tian Jin Kun Li Mei Li Zhi-Gang Ren Fu-Shun Wang Ji-Ye Zhu Xi-Sheng Leng Wei-Dong Yu |
author_sort | Zhong-Tian Jin |
collection | DOAJ |
description | Background: Overexpression of G-protein coupled receptor 34 (GPR34) affects the progression and prognosis of human gastric adenocarcinoma, however, the role of GPR34 in gastric cancer development and progression has not been well-determined. The current study aimed to investigate the effect of GPR34 knockdown on the proliferation, migration, and apoptosis of HGC-27 gastric cancer cells and the underlying mechanisms.
Methods: The expression of GPR34 in gastric cancer cell line HGC-27 was detected by quantitative real-time reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting. HGC-27 cells were employed to construct the stable GPR34 knockdown cell model in this study. Real-time RT-PCR and Western blotting were applied to validate the effect of short hairpin RNA (ShRNA) on the expression of GPR34 in HGC-27 gastric cells. The proliferation, migration of these cells were examined by Cell Counting Kit-8 and transwell. We also measured expression profile of PI3K/PDK1/AKT and ERK using Western blotting.
Results: The ShRNA directed against GPR34 effectively inhibited both endogenous mRNA and protein expression levels of GPR34, and significantly down-regulated the expression of PIK3CB (P < 0.01), PIK3CD (P < 0.01), PDK1 (P < 0.01), phosphorylation of PDK1 (P < 0.01), Akt (P < 0.01), and ERK (P < 0.01). Furthermore, GPR34 knockdown resulted in an obvious reduction in HGC-27 cancer cell proliferation and migration activity (P < 0.01).
Conclusions: GPR34 knockdown impairs the proliferation and migration of HGC-27 gastric cancer cells in vitro and provides a potential implication for therapy of gastric cancer. |
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institution | Directory Open Access Journal |
issn | 0366-6999 |
language | English |
last_indexed | 2024-12-22T21:31:07Z |
publishDate | 2015-01-01 |
publisher | Wolters Kluwer |
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series | Chinese Medical Journal |
spelling | doaj.art-fb7d38f8b6534ed4af8b63ee67909b6b2022-12-21T18:11:55ZengWolters KluwerChinese Medical Journal0366-69992015-01-01128454554910.4103/0366-6999.151114G-protein Coupled Receptor 34 Knockdown Impairs the Proliferation and Migration of HGC-27 Gastric Cancer Cells In VitroZhong-Tian JinKun LiMei LiZhi-Gang RenFu-Shun WangJi-Ye ZhuXi-Sheng LengWei-Dong YuBackground: Overexpression of G-protein coupled receptor 34 (GPR34) affects the progression and prognosis of human gastric adenocarcinoma, however, the role of GPR34 in gastric cancer development and progression has not been well-determined. The current study aimed to investigate the effect of GPR34 knockdown on the proliferation, migration, and apoptosis of HGC-27 gastric cancer cells and the underlying mechanisms. Methods: The expression of GPR34 in gastric cancer cell line HGC-27 was detected by quantitative real-time reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting. HGC-27 cells were employed to construct the stable GPR34 knockdown cell model in this study. Real-time RT-PCR and Western blotting were applied to validate the effect of short hairpin RNA (ShRNA) on the expression of GPR34 in HGC-27 gastric cells. The proliferation, migration of these cells were examined by Cell Counting Kit-8 and transwell. We also measured expression profile of PI3K/PDK1/AKT and ERK using Western blotting. Results: The ShRNA directed against GPR34 effectively inhibited both endogenous mRNA and protein expression levels of GPR34, and significantly down-regulated the expression of PIK3CB (P < 0.01), PIK3CD (P < 0.01), PDK1 (P < 0.01), phosphorylation of PDK1 (P < 0.01), Akt (P < 0.01), and ERK (P < 0.01). Furthermore, GPR34 knockdown resulted in an obvious reduction in HGC-27 cancer cell proliferation and migration activity (P < 0.01). Conclusions: GPR34 knockdown impairs the proliferation and migration of HGC-27 gastric cancer cells in vitro and provides a potential implication for therapy of gastric cancer.http://www.cmj.org/article.asp?issn=0366-6999;year=2015;volume=128;issue=4;spage=545;epage=549;aulast=JinGastric Cancer; GPR34; Knockdown; Migration; Proliferation |
spellingShingle | Zhong-Tian Jin Kun Li Mei Li Zhi-Gang Ren Fu-Shun Wang Ji-Ye Zhu Xi-Sheng Leng Wei-Dong Yu G-protein Coupled Receptor 34 Knockdown Impairs the Proliferation and Migration of HGC-27 Gastric Cancer Cells In Vitro Chinese Medical Journal Gastric Cancer; GPR34; Knockdown; Migration; Proliferation |
title | G-protein Coupled Receptor 34 Knockdown Impairs the Proliferation and Migration of HGC-27 Gastric Cancer Cells In Vitro |
title_full | G-protein Coupled Receptor 34 Knockdown Impairs the Proliferation and Migration of HGC-27 Gastric Cancer Cells In Vitro |
title_fullStr | G-protein Coupled Receptor 34 Knockdown Impairs the Proliferation and Migration of HGC-27 Gastric Cancer Cells In Vitro |
title_full_unstemmed | G-protein Coupled Receptor 34 Knockdown Impairs the Proliferation and Migration of HGC-27 Gastric Cancer Cells In Vitro |
title_short | G-protein Coupled Receptor 34 Knockdown Impairs the Proliferation and Migration of HGC-27 Gastric Cancer Cells In Vitro |
title_sort | g protein coupled receptor 34 knockdown impairs the proliferation and migration of hgc 27 gastric cancer cells in vitro |
topic | Gastric Cancer; GPR34; Knockdown; Migration; Proliferation |
url | http://www.cmj.org/article.asp?issn=0366-6999;year=2015;volume=128;issue=4;spage=545;epage=549;aulast=Jin |
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