ABSTRACT
Objective:To explore the effects of long non-coding RNA SATB2-AS1 in the proliferation and apoptosis of cervical cancer cells as an endogenous competitive RNA to regulate miR-373-5p/BTG3 axis.Methods:qRT-PCR was used to detect the expression of LncRNA SATB2-AS1, miR-373-5p and BTG3 in paracancerous tissue and cancerous tissue of patients with CC. The interaction between LncRNA SATB2/miR-373-5p/BTG3 was then predicted and verified. The expression of SATB2-AS1 and miR-373-5p in cells was intervened, subsequently the CC cells were divided into different groups. The proliferation activity of cells in each group was detected by MTT, and the apoptosis of cells in each group was detected by flow cytometry.Results:qRT-PCR showed that the expression of SATB2-AS1 and BTG3 in cancer tissue and CC cells was significantly decreased, while the expression of miR-373-5p was significantly increased in cancer tissue and CC cells compared with paracancerous tissue and normal cervical cells.The targeting relationship between SATB2-AS1 and miR-373-5p was confirmed. Compared with NC group, overexpression of SATB2-AS1 inhibited cell proliferation butinduced apoptosis. Overexpression of miR-373-5p promoted cell proliferation, inhibited apoptosis, but this effect was partially saved by SATB2-AS1.Conclusion:Up-regulation of LncRNA SATB2-AS1 expression regulated the miR-373-5p/BTG3 axis and participated in the progression of cervical cancer, subsequently inhibited cancer cell proliferation but induced apoptosis.
ABSTRACT
Objective To clarify the clinicopathological significance and the reversing effects of BTG3 expression on the aggressive phenotype in gastric cancer. Methods BTG3 expression was detected in gastric cancer tissues by on tissue microarray and immunostaining. BTG3?expressing plasmid was transfected into MKN28 and MGC803 cells,the proliferation,cell cycle,differentiation and autophagy were analyzed by CCK?8,PI staining,alkaline phosphatase activity and GFP?LC?3B transfection,respectively. Results BTG3 overexpression inhibited cell proliferation,in?duced S/G2 arrest,differentiation and autophagy in both cells(P<0.05). BTG3 expression was decreased in gastric cancer in comparison with the adjacent mucosa(P<0.05),and positively correlated with venous invasion and dedifferentiation of the cancers(P<0.05). Conclusion BTG3 ex?pression contributes to gastric carcinogenesis and subsequent progression. BTG3 overexpression can reverse the aggressive phenotypes,which could be employed as a potential target for gene therapy of gastric cancer.