2. Academic Validation
  3. RNF106 aggravates esophageal squamous cell carcinoma progression through LATS2/YAP axis

RNF106 aggravates esophageal squamous cell carcinoma progression through LATS2/YAP axis

  • Arch Biochem Biophys. 2023 May 17;109640. doi: 10.1016/j.abb.2023.109640.
Qifeng Sun 1,  Hongda Lu 1,  Wenjie Zhang 2,  Yang Du 3,  Qian Liang 3,  Yehui Zhang 3,  Jing Wu 4,  Mingwei Zhong 5
Affiliations

Affiliations

  • 1 Department of Thoracic Surgery, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.
  • 2 Department of General Surgery, The First Affiliated Hospital of Shandong First Medical University, Shandong Provincial Qianfoshan Hospital, Jinan, China.
  • 3 Department of Pharmacy, The First Affiliated Hospital of Shandong First Medical University, Shandong Provincial Qianfoshan Hospital, Jinan, China.
  • 4 Department of Pharmacy, The First Affiliated Hospital of Shandong First Medical University, Shandong Provincial Qianfoshan Hospital, Jinan, China. Electronic address: [email protected].
  • 5 Department of General Surgery, The First Affiliated Hospital of Shandong First Medical University, Shandong Provincial Qianfoshan Hospital, Jinan, China. Electronic address: [email protected].
PMID: 37207933 DOI: 10.1016/j.abb.2023.109640
Abstract

Esophageal squamous cell carcinoma (ESCC) is one of the most lethal solid tumors in China, with the 5-year overall survival rate less than 20%. Although the carcinogenic process of ESCC is still not clear, recent studies using whole genomic profiling revealed that dysregulation of Hippo signaling pathway might play important roles in ESCC progression. The ubiquitin-like with PHD and RING finger domain 1 (RNF106) was a modifier of DNA methylation and histone ubiquitination. In this study, we evaluate the oncogenic function of RNF106 in ESCC both in vitro and in vivo. Wound healing and transwell data showed that RNF106 was required for ESCC cell migration and invasion. RNF106 depletion dramatically restrained Hippo signaling targeted gene expression. The bioinformatics analysis displayed that RNF106 was increased in ESCC tumor tissues and related with poor survival in ESCC patients. Mechanistic studies demonstrated that RNF106 was associated with LATS2 and facilitate LATS2 K48-linked ubiquitination and degradation, which subsequently inhibited YAP phosphorylation and promoted YAP oncogenic function in ESCC. Taken together, our study revealed a novel link between RNF106 and Hippo signaling in ESCC, suggesting that RNF106 could be a promising target for ESCC therapy.

Keywords

ESCC; Hippo; LATS2; RNF106; Ubiquitination.

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