Open AccessCircular RNA circMAN2B2 promotes growth and migration of gastric cancer cells by down‐regulation of miR‐145
Author(s) -
Sun Bo,
Sun Haiyuan,
Wang Qunying,
Wang Xinhong,
Quan Jingzi,
Dong Dongfang,
Lun Yue
Publication year - 2020
Publication title -
journal of clinical laboratory analysis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.536
H-Index - 50
eISSN - 1098-2825
pISSN - 0887-8013
DOI - 10.1002/jcla.23215
Subject(s) - pi3k/akt/mtor pathway , oncogene , protein kinase b , transfection , western blot , viability assay , cancer research , apoptosis , biology , cell migration , microbiology and biotechnology , chemistry , cell , signal transduction , cell cycle , cell culture , gene , genetics
Background CircMAN2B2 is a newly discovered circRNA that has been found to be an oncogene in lung cancer and glioma. The present study was designed to reveal the role of circMAN2B2 in gastric carcinoma (GC). Methods qRT‐PCR method was utilized to examine circMAN2B2 expression in GC tissues and paracancerous tissues. Next, circMAN2B2 expression in SNU‐16 and AGS cells was silenced by transfection. CCK‐8 assay, colony formation assay, flow cytometer, Transwell assay, and Western blot were conducted for testing cell phenotype changes. Further, the downstream genes and signaling were uncovered by qRT‐PCR and Western blot. Results As relative to paracancerous tissues, circMAN2B2 was high‐expressed in GC tissues. Silence of circMAN2B2 clearly declined SNU‐16 and AGS cells viability, survival, migration but enhanced apoptosis. Meanwhile, silence of circMAN2B2 induced the cleavage of caspases (−3 and −9), down‐regulation of MMPs (−2 and −9), and up‐regulation of miR‐145. The impacts of circMAN2B2 silence toward SNU‐16 and AGS cells were attenuated by miR‐145 silence. Moreover, circMAN2B2 silence deactivated PI3K, AKT while activated JNK through regulating miR‐145. Conclusion This work presented the oncogenic function of circMAN2B2 in GC cells growth and migration. CircMAN2B2 exerted its function possibly through regulating miR‐145 as well as PI3K/AKT and JNK pathways.