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GNG12 overexpression inhibits triple-negative breast cancer cell proliferation, migration, and invasion  ( SCI-EXPANDED收录)  

文献类型:期刊文献

英文题名:GNG12 overexpression inhibits triple-negative breast cancer cell proliferation, migration, and invasion

作者:Shan, Biao-Feng[1,2];Zhao, Le[3,4];Hu, Tao[5];Xu, Jing-Hao[6];Zeng, Tong-Xu[2];Tang, Jian-Ming[1,7];Yu, Bo[2,3]

第一作者:Shan, Biao-Feng

通信作者:Tang, JM[1];Yu, B[2];Yu, B[3];Tang, JM[4]

机构:[1]Lanzhou Univ, Clin Med Coll 1, Lanzhou, Peoples R China;[2]Second Peoples Hosp Lanzhou, Gen Surg, Lanzhou, Peoples R China;[3]Gansu Univ Chinese Med, Clin Med Coll 1, Lanzhou, Peoples R China;[4]Xi An Jiao Tong Univ, Xibei Hosp, Affiliated Hosp 2, Xian, Peoples R China;[5]Zigong Fourth Peoples Hosp, Zigong, Peoples R China;[6]Zouping Peoples Hosp, Breast Surg, Binzhou, Peoples R China;[7]Lanzhou Univ, Hosp 1, Lanzhou, Peoples R China

第一机构:Lanzhou Univ, Clin Med Coll 1, Lanzhou, Peoples R China

通信机构:[1]corresponding author), Lanzhou Univ, Clin Med Coll 1, Lanzhou, Peoples R China;[2]corresponding author), Second Peoples Hosp Lanzhou, Gen Surg, Lanzhou, Peoples R China;[3]corresponding author), Gansu Univ Chinese Med, Clin Med Coll 1, Lanzhou, Peoples R China;[4]corresponding author), Lanzhou Univ, Hosp 1, Lanzhou, Peoples R China.|[10735]甘肃中医药大学;

年份:2026

卷号:16

期号:1

外文期刊名:SCIENTIFIC REPORTS

收录:;Scopus(收录号:2-s2.0-105047733666);WOS:【SCI-EXPANDED(收录号:WOS:001852875800001)】;

基金:This work was supported by the Lanzhou Science and Technology Planning Project (N0:2023-4-13), the Gansu Province Science and Technology Plan Project (22JR5RA1068) and Scientific Research Projects in the Health and Healthcare Sector of Lanzhou City (A2024030).

语种:英文

外文关键词:GNG12; Pan-cancer; Prognosis; Triple-negative breast cancer

摘要:Guanine nucleotide-binding protein subunit gamma-12 (GNG12), a G protein gamma-subunit, has been identified as a potential regulator of tumor biology. However, its functional relevance in triple-negative breast cancer (TNBC) remains unclear. In this study, we integrated pan-cancer transcriptomic analyses with experimental validation in TNBC models to investigate the expression patterns, clinicopathological significance, and biological roles of GNG12. GNG12 was found to be broadly downregulated across diverse cancer types, and its reduced expression was significantly associated with unfavorable patient survival outcomes. Low GNG12 expression correlated with adverse clinicopathological features in breast cancer (BRCA). Moreover, it was associated with poorer outcomes in TNBC patient cohorts. Functional assays demonstrated that GNG12 overexpression inhibited TNBC cell proliferation, migration, and invasion, whereas GNG12 knockdown exerted the opposite effects. Pathway analysis and western blotting indicated that GNG12 expression was associated with altered PI3K/AKT pathway activity. Additionally, mutations at S2 and S33-both located within predicted phosphorylation sites-were identified as candidate regulatory alterations whose functional relevance requires further validation. Moreover, GNG12 expression was positively correlated with RNA methylation-related markers and inversely associated with promoter methylation. Taken together, GNG12 was downregulated in TNBC and associated with suppression of malignant cellular phenotypes; however, its clinical significance and mechanistic relationship with PI3K/AKT signaling require further validation in larger cohorts and additional experimental models.

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