Inhibition of SOCS6 confers radioresistance in esophageal squamous cell carcinoma

Esophageal cancer is one of the most common cancer of the digestive system and radiotherapy is widely applied in advanced esophageal cancer treatment, however radioresistance (RR) is one of the major reasons for radiotherapy failure. There is limited knowledge on the mechanisms that cause RR, here we identify suppressors of cytokine signaling 6 (SOCS6) is a negative regulator of radioresistance in ESCC cells. SOCS6 deficiency in ESCC cells conferred radioresistance in vitro and in vivo by increasing radiation-induced G2/M arrest, DNA damage repair and inhibiting radiation-induced apoptosis. Moreover, the transcriptome sequencing analysis demonstrates that the transcription of SOCS6 was partially p53-dependent. Importantly we found that highly correlated SOCS6 and P53 express lower in RR esophageal cancer tissues compare with radiosensitive ones. Collectedly our study uncovers that SOCS6, as a downstream effector of p53, is a key regulator involved in the radioresistance of ESCC. (C) 2021 Elsevier Inc. All rights reserved.

Automated summary

SOCS6 deficiency in esophageal cancer cells leads to radioresistance by promoting radiation-induced G2/M arrest, DNA damage repair, and inhibiting apoptosis, which is partially dependent on p53 transcription. Lower expression of SOCS6 and P53 is correlated with radioresistant esophageal cancer tissues.