Published online Jun 21, 2021. doi: 10.3748/wjg.v27.i23.3327
Peer-review started: December 14, 2020
First decision: December 27, 2020
Revised: January 6, 2021
Accepted: May 19, 2021
Article in press: May 19, 2021
Published online: June 21, 2021
Processing time: 185 Days and 22.1 Hours
Core Tip: Tuftelin1 (TUFT1) has been reported to be regulated by hypoxia and involved in the Hedgehog signaling pathway, with over-expression in hepatocellular carcinoma (HCC) tissues or cell lines. Abnormal TUFT1 level was significantly related to tumor size, vascular invasion, positive hepatitis B e-antigen, advanced tumor-node-metastasis stage of HCC, patients with ascites, and shorter overall survival and disease-free survival. Interfering TUFT1 transcription could markedly suppress the growth and metastasis of high TUFT1 MHCC-97H cell lines in vitro through accelerating apoptosis. Moreover, increasing TUFT1 expression might promote the growth and metastasis of low TUFT1 Hep3B cell lines in vitro. The data suggested that TUFT1 is involved in HCC progression via the mechanism of inhibiting apoptosis and might serve as a potential therapeutic target for inhibiting HCC growth.
