2. Academic Validation
  3. MOB1A regulates glucose deprivation-induced autophagy via IL6-STAT3 pathway in gallbladder carcinoma

MOB1A regulates glucose deprivation-induced autophagy via IL6-STAT3 pathway in gallbladder carcinoma

  • Am J Cancer Res. 2020 Nov 1;10(11):3896-3910.
Bo Yang 1,  Yang Li 2 3 4,  Rui Zhang 5,  Liguo Liu 2 3 4,  Huijie Miao 2 3 4,  Yongsheng Li 2 3 4,  Ziyu Shao 2 3 4,  Tai Ren 2 3 4,  Yijian Zhang 2 3 4,  Qiyu Zhang 1,  Yingbin Liu 2 3 4,  Hongqi Shi 1
Affiliations

Affiliations

  • 1 Key Laboratory of Diagnosis and Treatment of Severe Hepato-Pancreatic Diseases of Zhejiang Province, Department of Surgery, First Affiliated Hospital of Wenzhou Medical University Baixiang Road, Wenzhou 325000, China.
  • 2 Department of General Surgery Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine Shanghai, China.
  • 3 Department of Biliary-Pancreatic Surgery Renji Hospital Affiliated to Shanghai Jiao Tong University School of Medicine Shanghai, China.
  • 4 Shanghai Key Laboratory of Biliary Tract Disease Research Shanghai, China.
  • 5 Department of Hepatobiliary Surgery, The First Affiliated Hospital of Xi'an Jiaotong University 277 West Yanta Road, Xi'an 710061, Shaanxi, China.
PMID: 33294275
Abstract

MOB kinase activator 1A (MOB1A) plays an important role in many diseases and cancers. Here, we observed that MOB1A was substantially overexpressed in gallbladder carcinoma (GBC) tissues compared with nontumor tissues. The high expression of MOB1A was closely associated with poor survival in patients with GBC at advanced TNM stages. Furthermore, our study indicated that MOB1A promoted Autophagy by activating the IL6/STAT3 signaling pathway and regulating the chemosensitivity to gemcitabine under glucose deprivation conditions both in vitro and in vivo. In conclusion, these findings suggested that MOB1A is critical for the development of GBC via the MOB1A-IL6/STAT3-autophagy axis.

Keywords

IL6-STAT3 pathways; MOB1A; autophagy; gallbladder carcinoma; glucose-deprivation.

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