详情页 - 聚合机构库演示平台

当前位置：首页 > 详情页

GPR168 functions as a tumor suppressor in mouse melanoma by restraining Akt signaling pathway

文献详情

资源类型：

Pubmed体系：

作者：

单位： [1]Shanxi Academy of Medical Sciences, Shanxi Bethune Hospital, Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, Taiyuan, China. [2]Tongji Medical College, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China. [3]Department of General Surgery, Chinese Academy of Medical Sciences, Shanxi Province Cancer Hospital, Shanxi Hospital Affiliated to Cancer Hospital, Cancer Hospital Affiliated to Shanxi Medical University, Taiyuan, China. [4]Tianjin First Central Hospital, Tianjin, China. [5]College of Veterinary Medicine, Institute of Animal Biotechnology, Shanxi Agricultural University, Taigu, Jinzhong, China. [6]Department of Blood Transfusion, Shanxi Provincial People's Hospital, Affiliate of Shanxi Medical University Taiyuan, Taiyuan, Shanxi, China.

出处：

DOI：

摘要：

Malignant melanoma (MM) is a malignant tumor associated with high mortality rates and propensity for metastasis. Despite advancement in treatment, the incidence of MM continue to rise globally. GPR168, also known as MrgprF, is a MAS related GPR family member. The low expression of GPR168 has also been reported in many malignant tumors including MM. In the study, the statistical analysis from The Cancer Genome Atlas (TCGA) revealed a significant down regulation of GPR168 in melanoma compared to normal melanocytes, underscoring its importance in MM. The aim of the present study is to investigate the affect of GPR168 overexpression and elucidate its molecular mechanisms in MM cells. In addition, we used mouse melanoma B16-F10 cell line and xenograph tumor model to explore the function of GPR168 in melanoma. Our findings demonstrate that GPR168 overexpression could inhibit B16-F10 cell proliferation, migration, and xenografts tumor growth. Further, mechanistic studies revealed that GPR168 affected B16-F10 progress through Akt signal pathway with the decreased expression of p-Akt, p-GSK-3β, β-catenin, Myc, CyclinD1 and CDK4. In order to validate these findings, a rescue experiment was formulated employing GPR168 polyclonal antibody (Anti-GPR168 pAbs) to block GPR168 functionality. The addition of Anti-GPR168 pAbs into the culture medium restored both cell proliferation and migration. In conclusion, the overexpression of GPR168 in mouse melanoma B16-F10 cells suppressed proliferation and migration through the Akt signaling pathway. These findings collectively propose GPR168 as a promising novel tumor suppressor in MM, suggesting its potential as a therapeutic target in future interventions.Copyright: © 2024 Guo et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

基金：

语种：

PubmedID：

中科院(CAS)分区：

出版当年[2023]版：

大类 | 3 区综合性期刊

小类 | 3 区综合性期刊

最新[2025]版：

大类 | 3 区综合性期刊

小类 | 3 区综合性期刊

第一作者：

第一作者单位： [1]Shanxi Academy of Medical Sciences, Shanxi Bethune Hospital, Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, Taiyuan, China. [2]Tongji Medical College, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China.

通讯作者：

通讯机构： [1]Shanxi Academy of Medical Sciences, Shanxi Bethune Hospital, Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, Taiyuan, China. [2]Tongji Medical College, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China.

推荐引用方式(GB/T 7714)：

APA：

MLA：