NEAT1 promotes cell proliferation in multiple myeloma by activating PI3K/AKT pathway
The role of long-chain non-coding NEAT1 (Nuclear enriched abundant transcript1) in multiple myeloma (MM) and its underlying mechanisms were investigated. The expression of NEAT1 and SOX13 was detected in CD138+ positive cells collected from MM and healthy subjects. Meanwhile, the relationship betwee...
Saved in:
Published in | European review for medical and pharmacological sciences Vol. 22; no. 19; p. 6403 |
---|---|
Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
Italy
01.10.2018
|
Subjects | |
Online Access | Get more information |
Cover
Loading…
Summary: | The role of long-chain non-coding NEAT1 (Nuclear enriched abundant transcript1) in multiple myeloma (MM) and its underlying mechanisms were investigated.
The expression of NEAT1 and SOX13 was detected in CD138+ positive cells collected from MM and healthy subjects. Meanwhile, the relationship between NEAT1 level and the prognosis as well as clinical staging was analyzed. Virus transfection method was used to change the expression of NEAT1 and SOX13 in tumor cells, and then the effect of NEAT1 on cell proliferation, apoptosis and cell cycle was examined. The influence of NEAT1 on the regulation of SOX13 was explored through recovery experiments and Western blot. In addition, the regulation effect of NEAT1 on tumor formation was explored in vivo.
NEAT1 and SOX13 were highly expressed in MM patients and MM cell lines, and the patient survival rate and platelet count were significantly decreased in the highly expressed NEAT1 group. Low expression of NEAT1 could inhibit the PI3K/AKT pathway to suppress cell proliferation, promote apoptosis, and inhibit cell cycle. Overexpression of SOX13 was able to partially restore the inhibitory effect of NEAT1 on cell proliferation. Meanwhile, it was found that low expression of NEAT1 significantly inhibited tumor formation in vivo.
Highly expressed NEAT1 promoted cell proliferation through activation of PI3K/AKT pathway, thus participating in the development of MM. |
---|---|
ISSN: | 2284-0729 |
DOI: | 10.26355/eurrev_201810_16053 |