The m6A demethylase ALKBH5-mediated upregulation of DDIT4-AS1 maintains pancreatic cancer stemness and suppresses chemosensitivity by activating the mTOR pathway

• Published in: Molecular cancer Vol. 21; no. 1; pp. 1 - 174
• Main Authors: Zhang, Yi, Liu, Xiaomeng, Wang, Yan, Lai, Shihui, Wang, Zhiqian, Yang, Yudie, Liu, Wenhui, Wang, Hongquan, Tang, Bo
• Format: Journal Article
• Language: English
• Published: London BioMed Central Ltd 02.09.2022; BioMed Central; BMC
• Subjects: ALKBH5; Animal models; Antibodies; Binding sites; Bioinformatics; Cancer; Care and treatment; Chemoresistance; Chemosensitivity; Chemotherapy; DDIT4-AS1; DNA damage; Drug resistance; Flow cytometry; Gemcitabine; Growth factors; HuR protein; Hypoxia; Immunoprecipitation; Medical prognosis; Methyltransferases; Molecular modelling; mRNA stability; N6-methyladenosine; Pancreatic cancer; Patients; Phosphorylation; Prognosis; Proteins; RNA; RNA sequencing; Scientific equipment and supplies industry; Stemness; TOR protein; Tumors; UPF1; Xenografts; United States; China; Grand Island New York; St Louis Missouri; United States > US; Germany

Abstract Background Chemoresistance is a major factor contributing to the poor prognosis of patients with pancreatic cancer, and cancer stemness is one of the most crucial factors associated with chemoresistance and a very promising direction for cancer treatment. However, the exact molecular mechan...