详情页 - 四川省肿瘤医院知识库

当前位置：首页 > 详情页

EMP2 acts as a suppressor of melanoma and is negatively regulated by mTOR-mediated autophagy

110| 认领 | 导出 | 链接全文 |

文献详情

资源类型：

WOS体系：

Pubmed体系：

收录情况： ◇ SCIE

作者：

机构： [1]State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Disease, Department of Orthodontics and Paediatrics, West China Hospital of Stomatology, Sichuan University, Chengdu, 610041, PR China [2]Department of Radiation Oncology, Sichuan Cancer Hospital & Institute, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Radiation Oncology Key Laboratory of Sichuan Province, Chengdu 610041, PR China [3]Department of Dermatology and State Key Laboratory of Biotherapy, West China Hospital, West China Medical School, Sichuan University, Chengdu 610041, PR China

出处：

DOI：

ISSN：

关键词： EMP2 mTOR Apoptosis Autophagy Melanoma

摘要：

Cutaneous melanoma is one of the most common malignant skin tumors and advanced melanoma is usually associated with a poor prognosis. In the current study, we demonstrated the tumor suppressing role of epithelial membrane protein-2 (EMP2) by inducing apoptosis in a A375 human melanoma cell line. Mechanistically, the low expression of EMP2 in melanoma is partially due to autophagic protein degradation mediated by the mTOR pathway. These results suggest there is regulation of autophagy as well as EMP2 levels might be an interesting novel targeted therapeutic strategy for melanoma. Although the further investigation is needed to deeply understand the regulatory mechanisms of EMP2 in melanoma progression and metastasis, our results clarify the functions and mechanisms of autophagy in melanoma, and shed new light on novel targeted therapeutics for melanoma.

基金：

语种：

被引次数：

WOS：

PubmedID：

中科院(CAS)分区：

出版当年[2019]版：

大类 | 3 区医学

小类 | 4 区肿瘤学

最新[2023]版：

大类 | 3 区医学

小类 | 4 区肿瘤学

JCR分区：

出版当年[2019]版：

Q2 ONCOLOGY

最新[2023]版：

Q2 ONCOLOGY

影响因子： 3.3 最新[2023版] 3.3 最新五年平均 3.565 出版当年[2019版] 3.558 出版当年五年平均 3.182 出版前一年[2018版] 4.207 出版后一年[2020版]

第一作者：

第一作者机构： [1]State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Disease, Department of Orthodontics and Paediatrics, West China Hospital of Stomatology, Sichuan University, Chengdu, 610041, PR China

共同第一作者：

通讯作者：

推荐引用方式(GB/T 7714)：

APA：

MLA：

相关文献

[1]Identification and optimization of 3-bromo-N'-(4-hydroxybenzylidene)-4-methylbenzohydrazide derivatives as mTOR inhibitors that induce autophagic cell death and apoptosis in triple-negative breast cancer. [2]Fangchinoline exerts anticancer effects on colorectal cancer by inducing autophagy via regulation AMPK/mTOR/ULK1 pathway. [3]Fluoxetine as a Potential Therapeutic Agent for Inhibiting Melanoma Brain and Lung Metastasis: Induction of Apoptosis, G0/G1 Cell Cycle Arrest, and Disruption of Autophagy Flux [4]Inhibition of TNBC Cell Growth by Paroxetine: Induction of Apoptosis and Blockage of Autophagy Flux [5]Pimavanserin tartrate induces apoptosis and cytoprotective autophagy and synergizes with chemotherapy on triple negative breast cancer [6]A novel mitochondria-targeting compound exerts therapeutic effects against melanoma by inducing mitochondria-mediated apoptosis and autophagy in vitro and in vivo [7]Detoxified pneumolysin derivative ΔA146Ply inhibits autophagy and induces apoptosis in acute myeloid leukemia cells by activating mTOR signaling. [8]BCLB, methylated in hepatocellular carcinoma, is a starvation stress sensor that induces apoptosis and autophagy through the AMPK-mTOR signaling cascade [9]Pseudolaric acid B suppresses NSCLC progression through the ROS/AMPK/mTOR/autophagy signalling pathway [10]Parthenolide Inhibits the Proliferation of MDA-T32 Papillary Thyroid Carcinoma Cells in Vitro and in Mouse Tumor Xenografts and Activates Autophagy and Apoptosis by Downregulation of the Mammalian Target of Rapamycin (mTOR)/PI3K/AKT Signaling Pathway