- Author:
Ying WANG
1
;
Wei SANG
1
;
Cai SUN
1
;
Ling-Yu ZENG
1
;
Kai-Lin XU
2
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; Cell Proliferation; Humans; Jurkat Cells; Lentivirus; MicroRNAs; NF-kappa B; Phosphatidylinositol 3-Kinases; Signal Transduction; Transfection; Up-Regulation
- From: Journal of Experimental Hematology 2015;23(1):94-98
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVEThis study was to investigate the effect of has-miR-150 on the proliferation and apoptosis in human acute T lymphocytic leukemia (T-ALL) cell line Jurkat, and explore its mechanism.
METHODSLentivirus-has-miR-150 was constructed and transfected to Jurkat cells. The expression of miR-150 was detected by real time PCR; the cell proliferation and apoptosis were detected by CCK-8 method and Annexin V/7-AAD labeling, respectively; the cell-related protein expressions of phosphatidylinositol-3-kinase(PI3K)/serine/ threonine kinase (Akt) signaling pathway were detected by Western blot.
RESULTSThe expression of miR-150 in infected Jurkat cells was significantly upregulated by constructing lentivirus-has-miR-150. Compared to negative control (transfected with empty-vector lentivirus), the cell proliferation after LV-miR-150 transfection was significantly inhibited and cell apoptosis was remarkably induced. Phosphorylation levels of P13K/Akt/NF-κB signaling pathway protein p-Akt and p-p65 decreased,whereas no obvious change was found in the expression of Akt.
CONCLUSIONmiR-150 may be a putative oncoprotein in T-ALL cells. Overexpression of miR-150 has noticeable effects on the proliferation inhibition and apoptosis induction of Jurkat cells, which may be mediated by the negative regulation of PI3K/Akt /NF-κB signaling pathway.