Home FOR AUTHORS Neoplasma 2021 Neoplasma Vol.68, No.2, p.362–374, 2021

Journal info


6 times a year.
Founded: 1954
ISSN 0028-2685
ISSN 1338-4317 (online)

Published in English

Editorial Info
Abstracted and Indexed
Submission Guidelines

Select Journal







Webshop Cart

Your Cart is currently empty.

Info: Your browser does not accept cookies. To put products into your cart and purchase them you need to enable cookies.

Neoplasma Vol.68, No.2, p.362–374, 2021

Title: LncRNA MEG3 promotes endoplasmic reticulum stress and suppresses proliferation and invasion of colorectal carcinoma cells through the MEG3/miR-103a-3p/PDHB ceRNA pathway
Author: Youguang Huang, Fujia Xie, Xi Cheng, Junlin Chi, Yi Lei, Rong Guo, Jiangqiong Han

Abstract: LncRNA maternally expressed gene 3 (MEG3) is a potential prognostic and diagnostic biomarker in colorectal carcinoma (CC). However, its cellular functions and mechanism remain not fully uncovered.
Relative expression of MEG3, miRNA (miR)-103a-3p, and pyruvate dehydrogenase E1 subunit beta (PDHB) was detected by RT-qPCR and western blotting. Cell proliferation was measured by CCK-8 assay, colony formation assay, and flow cytometry, as well as xenograft tumor assay. Transwell assay examined cell invasion. Endoplasmic reticulum (ER) stress was evaluated by western blotting. Dual-luciferase reporter assay and RNA immunoprecipitation determined the relationship between miR-103a-3p and MEG3 or PDHB. Expression of MEG3 was downregulated in human CC tumor tissues and cells (SW620 and HCT116), accompanied by higher miR-103a-3p and lower PDHB. Restoring MEG3 suppressed cell viability, colony formation ability, and invasion, arrested cell cycle, and induced apoptosis rate in SW620 and HCT116 cells, as well as promoted expression of ER stress-related proteins (GRP78, ATF6, CHOP, caspase-3, and caspase-9). Furthermore, MEG3 overexpression hindered tumor growth and facilitated ER stress in vivo. Molecularly, miR-103a-3p was a target of MEG3, and further targeted PDHB. Similarly, in function, blocking miR-103a-3p suppressed CC in vitro by affecting proliferation, invasion, and ER stress; in addition, restoring miR-103a-3p partially counteracted the suppressive role of MEG3 in CC cells.
MEG3 sponged miR-103a-3p to suppress CC malignancy by inducing ER stress and inhibiting cell proliferation and invasion via upregulating PDHB, suggesting a novel MEG3/miR-103a-3p/PDHB ceRNA pathway.

Keywords: MEG3; ER stress; miR-103a-3p; pyruvate dehydrogenase E1 subunit beta (PDHB); colorectal carcinoma
Published online: 29-Oct-2020
Year: 2021, Volume: 68, Issue: 2 Page From: 362, Page To: 374
doi:10.4149/neo_2020_200813N858


download file



© AEPress s.r.o
Copyright notice: For any permission to reproduce, archive or otherwise use the documents in the ELiS, please contact AEP.