Open AccessCircRHOT1 mediated cell proliferation, apoptosis and invasion of pancreatic cancer cells by sponging miR‐125a‐3p
Author(s) -
Ling Sunkai,
He Yanru,
Li Xiaoxue,
Hu Mingyue,
Ma Yu,
Li Yuan,
Lu Zipeng,
Shen Shanshan,
Kong Bo,
Zou Xiaoping,
Jiang Kuirong,
Huang Peilin
Publication year - 2020
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.15572
Subject(s) - pancreatic cancer , cancer research , apoptosis , cancer , gene knockdown , cancer cell , cell growth , biology , ca19 9 , cell culture , medicine , biochemistry , genetics
Pancreatic cancer patients are asymptomatic at early stages and leading to late diagnoses. Additionally, pancreatic cancer easily metastasizes and is resistant to radiotherapy and chemotherapy. Therefore, it is critical to understand the underlying molecular mechanisms involved in pancreatic cancer to develop more efficient diagnostic and treatment strategies. In this study, we demonstrated that circRHOT1 was overexpressed in pancreatic cancer tissues and cell lines, and it was found to directly bind to miR‐125a‐3p, acting as an endogenous sponge to inhibit its activity. Knockdown of circRHOT1 expression significantly inhibited proliferation as well as invasion, and it promoted apoptosis of pancreatic cancer cells via the regulation of E2F3 through the targeting of miR‐125a‐3p. Taken together, our results showed that circRHOT1 plays critical roles in regulating the biological functions of pancreatic cancer cells, suggesting that circRHOT1 may serve as a potential diagnostic marker and therapeutic target for patients with pancreatic cancer.