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FAST1 Predicts Poor Survival of Renal Carcinoma and Promotes Its Progression Through the TGF-β/Smad Pathway

Authors Tian T, Fu X, Hu L, Yang X, Sun P, Sun F

Received 26 October 2020

Accepted for publication 18 January 2021

Published 26 February 2021 Volume 2021:14 Pages 1487—1499

DOI https://doi.org/10.2147/OTT.S288847

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 3

Editor who approved publication: Dr Sanjeev Srivastava


Tao Tian,1 Xiangyang Fu,2 Liangliang Hu,1 Xiaofeng Yang,1 Peng Sun,1 Fengfeng Sun1

1Department of Urology, Zaozhuang Municipal Hospital, Zaozhuang, 277100, Shandong, People’s Republic of China; 2Zaozhuang Yicheng District People’s Hospital, Zaozhuang, Shandong, 277300, People’s Republic of China

Correspondence: Fengfeng Sun
Department of Urology, Zaozhuang Municipal Hospital, No. 41 Longtou Road, Shizhong District, Zaozhuang, 277100, Shandong, People’s Republic of China
Tel + 86 0632 3288037
Email [email protected]

Purpose: Renal carcinoma (RC) originates in the renal tubular epithelial system, among which renal cell carcinoma (RCC) is the most frequent one. The forkhead activin signal transducer 1 (FAST1) has been shown to interfere with tumor progression as an oncogene, while its role in RC is limited. Therefore, this paper explored the prognostic significance, specific effects, and related mechanisms of FAST1 on RC.
Patients and Methods: Cell colony formation assay, cell counting kit-8 (CCK8) assay, flow cytometry and Transwell assay were used to test cell proliferation, viability, apoptosis, migration and invasion, respectively. Western blot (WB) was employed to determine the protein level of FAST1.
Results: Our study confirmed that FAST1 was up-regulated in RC tissues and cell lines, and its overexpression often represented a poor prognosis of RC patients. Meanwhile, the in vitro experiments showed that overexpressing FAST1 facilitated RC cell viability, proliferation, migration, invasion and epithelial-mesenchymal transition (EMT), and repressed cell apoptosis. In addition, the in vivo experiments illustrated that the up-regulation of FAST1 strengthened tumor growth. On the contrary, knocking down FAST1 had the opposite effects. Mechanistically, The TGF-β/Smad pathway contributed to RC evolvement and was activated by FAST1 both in vitro and in vivo.
Conclusion: This article suggests that FAST1 exerts a carcinogenic role in RC by regulating the TGF-β/Smad signaling.

Keywords: forkhead activin signal transducer 1, TGF-β/Smad pathway, renal carcinoma

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