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Ribosomal protein L31 (RPL31) inhibits the proliferation and migration of gastric cancer cells.
Wu, Fang; Liu, Yangyang; Hu, Shenglin; Lu, Canrong.
Afiliação
  • Wu F; Department of Oncology, The First Affiliated Hospital of Nanchang University. Yongwaizheng Street, No. 17, Nanchang City, Jiangxi Province 330006, China.
  • Liu Y; Department of Oncology, The First Affiliated Hospital of Nanchang University. Yongwaizheng Street, No. 17, Nanchang City, Jiangxi Province 330006, China.
  • Hu S; Department of Internal Medicine, People's Hospital of Jinan County. Beida Street, No. 5, Jinan City, Jiangxi Province 330699, China.
  • Lu C; Senior Department of General Surgery, The First Medical Center of Chinese, PLA General Hospital. Fuxin Road, No. 28, Haidian District, Beijing 100853, China.
Heliyon ; 9(2): e13076, 2023 Feb.
Article em En | MEDLINE | ID: mdl-36816257
ABSTRACT
Gastric cancer (GC) is a digestive tract malignant tumor and causes the third cancer-related mortality in the world. Aberrant expression of Ribosomal Protein L31 (RPL31) has been reported in several human cancers. The aim of this study was to explore the role and possible biological functions of RPL31 in GC. We firstly employed immunohistochemistry to examine RPL31 expression in tumor and para-cancerous tissues. By lentiviral transfection, we successfully constructed an RPL31-knockdown GC cell model and performed functional validation to reveal the effects of RPL31 on proliferation, apoptosis, cycle, migration, and tumor growth. Our data indicated that RPL31 was abundantly expressed in GC tissues and cell lines (AGS and MGC-803). In addition, RPL31 expression was positively correlated with the extent of tumor infiltrate of GC patients. Functionally, silencing RPL31 in AGS and MGC-803 cells significantly limited the ability of proliferation and migration, promoted cell apoptosis. Consistently, RPL31-knockdown GC cells inhibited the growth of xenografts in mice. Moreover, preliminary analysis on the downstream regulation mechanism revealed that RPL31 functioned as a tumor promoter through targeting JAK-STAT signaling pathway. In conclusion, inhibition of abnormally high expression of RPL31 in GC may be a potential therapeutic strategy for this disease.
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Texto completo: 1 Base de dados: MEDLINE Idioma: En Revista: Heliyon Ano de publicação: 2023 Tipo de documento: Article País de afiliação: China

Texto completo: 1 Base de dados: MEDLINE Idioma: En Revista: Heliyon Ano de publicação: 2023 Tipo de documento: Article País de afiliação: China