Long Non-Coding Rna Small Nucleolar Rna Host Gene 1 And Microrna-100-3p Expression In Endometrial Carcinoma And Its Effect On The Proliferation And Apoptosis Of Ishikawa Cells

The aim of this study was to explore LncRNA SNHG1 and miRNA-100-3p expression in endometrial carcinoma and its effect on the proliferation and apoptosis of Ishikawa cells. A qRT-PCR assay was conducted to determine SNHG1 and miRNA-100-3p expression in endometrial cancer tissues and paracancerous tissues. Human endometrial cancer Ishikawa cells were cultured in vitro. Si-NC, si-SNHG1, si-SNHG1, anti-miRNA-NC, and si-SNHG1 were transfected into Ishikawa cells with anti-miRNA-519b-3p. A qRT-PCR assay was performed to determine SNHG1 and miRNA-100-3p expression, and the CCK-8 method was used to determine cell proliferation. Flow cytometry was conducted to determine cell cycle and apoptosis rate and a dual luciferase reporter experiment was carried out to test the targeting association between SNHG1 and miRNA-100-3p. Cleaved Caspase-3, CHOP, and ATF4 expression were determined with the Western Blot method. SNHG1 expression level and miRNA-519b-3p expression level were much higher and much lower, respectively, in endometrial cancer tissues than in paracancerous tissues (P < 0.05). Transfection of si-SNHG1 can greatly attenuate cell viability and S cell ratio (P < 0.05), and increase G0/G1 cell ratio, apoptosis rate, Cleaved Caspase-3, CHOP, and ATF4 protein level (P < 0.05) compared to the si-NC group. Furthermore, the double luciferase reporter experiment confirmed that SNHG1 can competitively combine with miRNA-100-3p. Also, co-transfection of si-SNHG1 and anti-miRNA100-3p could significantly increase cell viability and S cell ratio (P < 0.05), and decrease G0/G1 cell ratio and apoptosis rate, and Cleaved Caspase-3, CHOP, and ATF4 protein levels compared to si-SNHG1 + anti-miRNA-NC (P < 0.05). Interfering with SNHG1 could inhibit the proliferation of Ishikawa cells and promote apoptosis by upregulating miRNA-100-3p expression.