Research Paper Volume 13, Issue 16 pp 20179—20191
Long non-coding RNA ABHD11-AS1 promotes colorectal cancer progression and invasion through targeting the integrin subunit alpha 5/focal adhesion kinase/phosphoinositide 3 kinase/Akt signaling pathway
- 1 Department of Gastroenterology, Affiliated Sanming First Hospital of Fujian Medical University, Sanming 365000, Fujian, China
- 2 Department of Endoscope Room, Affiliated Sanming First Hospital of Fujian Medical University, Sanming 365000, Fujian, China
- 3 Department of Clinical Laboratory, Affiliated Sanming First Hospital of Fujian Medical University, Sanming 365000, Fujian, China
- 4 Department of Gynecology, Affiliated Sanming First Hospital of Fujian Medical University, Sanming 365000, Fujian, China
- 5 Department of Medical and Radiation Oncology, Affiliated Sanming First Hospital of Fujian Medical University, Sanming 365000, Fujian, China
Received: September 19, 2020 Accepted: July 6, 2021 Published: August 10, 2021
https://doi.org/10.18632/aging.203342How to Cite
Copyright: © 2021 Luo et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Long non-coding (lnc)RNA ABHD11-AS1 participates in the development and progress of various cancers, but its role in colorectal cancer (CRC) remains poorly known. In the present study, public database analysis and quantitative reverse transcription PCR of CRC and normal tissues showed that ABHD11-AS1 was overexpressed in CRC and associated with poor prognosis in CRC patients. Both in vitro and in vivo experiments demonstrated that loss-of-function of ABHD11-AS1 attenuated the proliferation, migration, and invasion of CRC cells and induced their apoptosis. Transcriptome sequencing and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis indicated that the phosphoinositide 3 kinase (PI3K)/Akt signaling pathway is a potential target of ABHD11-AS1. Additionally, we noted that ABHD11-AS1 deficiency reduced integrin subunit alpha (ITGA)5 expression, and impaired the phosphorylation of P85, focal adhesion kinase (FAK), and Akt1 in CRC cell lines and tumor tissues of nude mice. Furthermore, we observed that ITGA5 overexpression abrogated the effect of ABHD11-AS1 knockdown on the proliferation and invasion abilities of CRC cells. Taken together, our studies suggest that lncRNA ABHD11-AS1 promotes proliferation, migration, and invasion in CRC by activating the ITGA5/Fak/PI3K/Akt signaling pathway, and that the ITGA5/Fak/PI3K/Akt axis is a promising target for CRC therapy.