10.6084/M9.FIGSHARE.C.5129696.V1
Jun Tian
Jun
Tian
Peng Cui
Peng
Cui
Pudong Medical Center
Yifei Li
Yifei
Li
Changchun University of Chinese Medicine
Xuequan Yao
Xuequan
Yao
Nanjing University of Chinese Medicine
Xiaoyu Wu
Xiaoyu
Wu
Nanjing University of Chinese Medicine
Zhirong Wang
Zhirong
Wang
Chunsheng Li
Chunsheng
Li
0000-0002-6041-2854
China-Japan Friendship Hospital
LINC02418 promotes colon cancer progression by suppressing apoptosis via interaction with miR-34b-5p/BCL2 axis
Abstract Background LncRNAs act as functional regulators in tumor progression through interacting with various signaling pathways in multiple types of cancer. However, the effect of LINC02418 on colorectal cancer (CRC) progression and the underling mechanisms remain unclear. Methods LncRNA expression profile in CRC tissues was investigated by the TCGA database. The expressional level of LINC02418 in CRC patients was determined by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Kaplan–Meier analyses was used to investigate the correlation between LINC02418 and overall survival (OS) of CRC patients. Cell proliferative, migratory and invasive abilities were detected by CCK-8 assays, colony formation assays and trans-well assays in HCT116 and LoVo cells which were stably transduced with sh-LINC02418 or sh-NC. The binding between LINC02418 and miR-34b-5p, and the interaction between miR-34b-5p and BCL2 were determined by dual-luciferase assays. Western blot experiments were conducted to further explore the effect of miR-34b-5p on BCL2 signaling pathway. Rescue experiments were performed to uncover the role of LINC02418/miR-34b-5p/BCL2 axis in CRC progression. Results LINC02418 was upregulated in human colon cancer samples when compared with adjacent tissue, and its high expressional level correlated with poor prognosis of CRC patients. LINC02418 promoted cancer progression by enhancing tumor growth, cell mobility and invasiveness of colon cancer cells. Additionally, LINC02418 could physically bind to miR-34b-5p and subsequently affect BCL2 signaling pathway. Down-regulation of LINC02418 reduced cell proliferation, while transfection of miR-34b-5p inhibitor or BCL2 into LINC02418-silenced CRC cells significantly promoted CRC cells growth. Conclusions LINC02418 was upregulated in human CRC samples and could be used as the indicator for prediction of prognosis. LINC02418 acted as a tumor driver by negatively regulating cell apoptosis through LINC02418/miR-34b-5p/BCL2 axis in CRC.
Biophysics
Biochemistry
Microbiology
Cell Biology
Genetics
Molecular Biology
Chemical Sciences not elsewhere classified
Immunology
Biological Sciences not elsewhere classified
Cancer
figshare
2020
2020-09-23
2020-09-23
Collection
10.6084/m9.figshare.c.5129696
CC BY 4.0