Purpose: To investigate the function of LINC01170 in the progression of endometrial carcinoma and its underlying mechanism.
Methods: The expression profiles and prognostic data of endometrial carcinoma were downloaded by GDC (genomic data commons) analysis tools. Differentially expressed long noncoding (lnc)RNAs were analyzed by the edgeR (empirical analysis of digital gene expression data in R) package. LncRNAs that were related to prognosis of endometrial carcinoma were calculated by the survival function. Moreover, the PHEAT map package was introduced to edit heatmaps of differentially expressed lncRNAs. Human endometrial carcinoma cell lines (Ishikawa, ECC and HEC-IA) were cultured. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expressions of lncRNAs and related genes. Cell proliferation was detected by MTT, and cell cycle and apoptosis were detected by flow cytometry. Additionally, Western blot was used to detect protein expressions of relative genes.
Results: Results showed that LINC01170 was a non-coding RNA. LINC01170 was overexpressed in endometrial carcinoma, which was a risk factor for prognosis of this disease. LINC01170 expressions in carcinoma and para-cancerous tissues of 50 patients with endometrial carcinoma were detected by qRT-PCR and found that the expression level of LINC01170 in endometrial carcinoma was remarkably increased than that of para-cancerous tissues. Moreover, the expression level of LINC01170 in advanced endometrial carcinoma was remarkably higher than that of early-stage disease. After interfering with LINC01170, the proliferation of both the Ishikawa and HEC-1A cells were remarkably decreased, and cell cycle was arrested at the G0/G1 phase. Meanwhile, apoptosis results showed a remarkable apoptosis rate after interfering with LINC01170. Western blot results also demonstrated the decreased activity of AKT pathway and phosphorylated expression of AKT protein after LINC01170 knockdown. In addition, expressions of CDK2, CDK4 and Bcl-2 were decreased after LINC01170 knockdown.
Conclusions: LINC01170 promotes the progression of endometrial carcinoma through stimulating proliferation, cell cycle transition and inhibiting apoptosis of endometrial carcinoma cells via AKT pathway.