Effect of small ubiquitin-like modifier 1 pseudogene 3 on the proliferation and apoptosis of non-small cell lung cancer cell line H1299 through protein kinase B signaling pathway / 解剖学报

ABSTRACT

Objective To investigate the effect of long noncoding RNA (IncRNA) small ubiquitin-like modifier 1 pseudogene 3(SUM01P3) on the proliferation and apoptosis of non-small cell lung cancer cell line 1299. Methods Determination of SUM01P3 expression in non-small cell lung cancer cells by Real-time PCR. SUM01P3 small interfering RNA(siRNA) was transfected into H1299 cells, the down regulation effect was determined by Real-time PCR. Cell proliferation was measured by MTT, 5-ethynyl-2′-deoxyuridine(EdU) method, the cell cycle was determined by PI single staining, apoptosis was detected by annexin V -FITC/PI, detection of apoptosis by TUNEL, Western blotting was used to detect the expression of cleaved Caspase-3 (c-Caspase-3), cyclin Dl, P27, phosphorylated phospoinositide 3-kinase (p-PI3K) and phosphorylated protein kinase B (p-Akt). Akt signal activator treated H1299 cells transfected with SUM01P3 siRNA, cell proliferation, apoptosis and cycle change were also measured by the above methods. The number of samples was 9. Results SUM01P3 was up-regulated in non-small cell lung cancer cells. The expression of SUM01P3 in H1299 cells decreased after transfection with SUM01P3 siRNA, cell proliferation decreased, the ratio of G0/Gj phase increased, apoptosis rate increased, c-Caspase-3 and P27 protein in the cells increased, the protein levels of cyclin D1, p-PI3K and p-Akt decreased. Akt signal activator could reverse the inhibition of proliferation, cycle arrest and apoptosis of H1299 cells by SUM01P3 siRNA. Conclusion Down-regulation of SUM01P3 inhibits the proliferation of non-small cell lung cancer H1299 cells and induces apoptosis, the mechanism of action is related to the reduction of the activation level of the Akt signaling pathway.