Smad4 induces cell death in HO-8910 and SKOV3 ovarian carcinoma cell lines via PI3K-mTOR involvement.

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Abstract

This study investigated the effect and mechanism of Smad4 in ovarian carcinoma (OC) cell viability and demonstrated that Smad4 acted as a tumor suppressor in OC, which may contribute to the understanding of molecular mechanisms underlying OC occurrence and progression. Smad4 expression was decreased in the OC specimens, but Smad4 recovery in the OC cell lines impaired the survival and viability of OC cells by increasing autophagy and apoptosis. Further investigation showed that Smad4 interacted with the P85 subunit of PI3K and caused deactivation of the PI3K/mTOR pathway. Therefore, Smad4 could be considered as a target in cancer therapy due to its regulatory effect in OC carcinogenesis.

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Author and article information

Journal

Journal ID (iso-abbrev): Exp Biol Med (Maywood)

Title: Experimental biology and medicine (Maywood, N.J.)

Publisher: SAGE Publications

ISSN (Electronic): 1535-3699

ISSN (Print): 1535-3699

Publication date (Electronic): May 2020

Volume: 245

Issue: 9

Affiliations

[1 ] Department of Gynecology, the Affiliated Hospital of Qingdao University, Qingdao 266000, People's Republic of China.

[2 ] Cell Biology & Genetics Department, Medical College, Qingdao University, Qingdao 266021, People's Republic of China.

[3 ] Henan Road Community Health Service Center, Qingdao 266021, People's Republic of China.

Article

DOI: 10.1177/1535370220916709

PMC ID: 7273890

PubMed ID: 32276544

SO-VID: ef754fe7-7e10-4016-b19b-2286c5db2fdf

History

Keywords: autophagy,Smad4,PI3K,Ovarian carcinoma,mTOR,apoptosis

Data availability:

Keywords: autophagy, Smad4, PI3K, Ovarian carcinoma, mTOR, apoptosis

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