Long noncoding RNA HAGLROS promotes the process of mantle cell lymphoma by regulating miR-100/ATG5 axis and involving in PI3K/AKT/mTOR signal.

Abstract

This research planned to grab the expression and impact of lncRNA HAGLROS in the biology and progression of mantle cell lymphoma. HAGLROS level in mantle cell lymphoma cell lines was detected, followed by investigation of the influences of HAGLROS silencing on Mino cell biological performances. Afterwards, the express patterns of HAGLROS vs. miR-100, as well as miR-100 vs. ATG5, were investigated. Furthermore, whether HAGLROS could regulate the signals of PI3K/AKT/mTOR was analyzed. HAGLROS level was high in mantle cell lymphoma cell lines. Silencing of HAGLROS inhibited Mino cell viability, increased apoptosis and decreased autophagy by sponging miR-100. Moreover, miR-100 targeted ATG5 fixed. Furthermore, HAGLROS suppression resulted in inhibition on the briskness of PI3K/AKT/mTOR signals. Concurrently HAGLROS suppression and miR-100 inhibitor markedly changed the impacts of HAGLROS down-regulation alone on activating PI3K/AKT/mTOR signals, which could further change after co-transfection of si-HAGLROS + miR-100 inhibitor + siATG5. Our findings point out that expression of HAGLROS is increased in mantle cell lymphoma cells and may function as an oncogene in mantle cell lymphoma. HAGLROS may promote tumour development by regulating miR-100/ATG5/PI3K/AKT/mTOR axis.

• Authors: Guangfu Mu, Qian Liu, Si Wu, Yong Xia, Qing Fang
• Journal: Artificial cells, nanomedicine, and biotechnology (Artif Cells Nanomed Biotechnol) Vol. 47 Issue 1 Pg. 3649-3656 (Dec 2019) ISSN: 2169-141X [Electronic] England
• PMID: 31498006 (Publication Type: Journal Article, Retracted Publication)

Chemical References

• Autophagy-Related Protein 5
• MIRN100 microRNA, human
• MicroRNAs
• RNA, Long Noncoding
• Proto-Oncogene Proteins c-akt
• TOR Serine-Threonine Kinases

Topics

• Autophagy-Related Protein 5 (genetics)
• Base Sequence
• Cell Line, Tumor
• Humans
• Lymphoma, Mantle-Cell (pathology)
• MicroRNAs (genetics)
• Phosphatidylinositol 3-Kinases (metabolism)
• Proto-Oncogene Proteins c-akt (metabolism)
• RNA, Long Noncoding (genetics)
• Signal Transduction (genetics)
• TOR Serine-Threonine Kinases (metabolism)