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Downregulation of SSR2 Enhances Hepatocellular Carcinoma Cisplatin Sensitivity via the Hippo Pathway

Authors :
Rong Ye
Ling Yin
Yilong Ge
Xiansen Zhu
Yuansheng Xiao
Cuifu Fang
Qingquan Liu
Honghui Zhang
Heping Li
Binhui Xie
Source :
Frontiers in Bioscience-Landmark, Vol 29, Iss 8, p 299 (2024)
Publication Year :
2024
Publisher :
IMR Press, 2024.

Abstract

Background: Chemotherapy resistance is an obstacle to promoting the survival of patients with hepatocellular carcinoma (HCC). Thus, finding promising therapeutic targets to enhance HCC chemotherapy is necessary. Methods: Signal sequence receptor subunit (SSR2) expression analysis was performed using quantitative real time polymerase chain reaction (qPCR) and Western blotting assays. Colony formation, apoptosis, anchorage-independent growth assay, and in vivo animal models were used to investigate the effect of SSR2 expression on the resistance of HCC cells to Cisplatin (DDP). Western blotting and luciferase reporter gene techniques were used to explore the molecular mechanism of SSR2 on the resistance of HCC cells to DDP. Results: We found that the SSR2 is upregulated in HCC and associated with poor survival. Further analysis showed that the downregulation of SSR2 increased the sensitivity of HCC to DDP. Mechanically, SSR2 inhibited the Yes-associated protein (YAP) phosphorylation and promoted the transcription of Hippo signaling downstream genes. Finally, the Hippo pathway inhibitor can suppress colony formation and tumorigenesis arising from SSR2 upregulation. Conclusions: Our study shows that SSR2 is important in HCC progression via the Hippo pathway. Thus, targeting the SSR2/Hippo axis might be a potential strategy for overcoming HCC resistance to DDP.

Details

Language :
English
ISSN :
27686701
Volume :
29
Issue :
8
Database :
Directory of Open Access Journals
Journal :
Frontiers in Bioscience-Landmark
Publication Type :
Academic Journal
Accession number :
edsdoj.fd3a3180963641bd83de3611cb2d9825
Document Type :
article
Full Text :
https://doi.org/10.31083/j.fbl2908299