Long Noncoding RNA HOTAIR Promotes Endometrial Carcinoma Cell Proliferation by Binding to PTEN via the Activating Phosphatidylinositol 3-Kinase/Akt Signaling Pathway

Abstract

Accumulating evidence has demonstrated that long noncoding RNAs (lncRNAs) exert essential biological functions in modulating the progression of endometrial carcinoma (EC). HOX transcript antisense intergenetic RNA (HOTAIR) has been widely recognized as a crucial mediator in various tumors, including EC. However, the specific molecular mechanism of HOTAIR in the development of EC remains to be further explored. In the present study, we demonstrated that HOTAIR was significantly upregulated in EC tissues; this was negatively correlated with PTEN but positively correlated with phosphatidylinositol 3-kinase (PI3K) and Akt. Overexpression of HOTAIR promoted proliferation and inhibited apoptosis of EC cells, similar to PTEN knockdown. Additionally, RNA pulldown demonstrated the direct binding relationship between HOTAIR and PTEN. Furthermore, HOTAIR activated the PI3K/Akt pathway to promote EC progression by suppressing PTEN in vivo. Taking these results together, we revealed that high expression of HOTAIR promoted cell proliferation and inhibited apoptosis through activating the PI3K/Akt pathway via binding to PTEN, which might provide a prognostic marker and therapeutic target of EC.

Long non‑coding RNA SNHG12 regulates cell proliferation, invasion and migration in endometrial cancer by targeting miR‑4429

“…In carcinoma cells, lncRNAs and miRNA can function as tumor suppressors or oncogenes. A recent study demonstrated that increased expression of the lncRNA HOX transcript antisense RNA may promote cell proliferation and inhibit apoptosis by binding to phosphatase and tensin homolog in EC, suggesting the important roles that lncRNAs serve in EC ( 9 ). Previous studies have demonstrated that small nucleolar RNA host gene 12 (SNHG12), a lncRNA transcribed from human chromosome 1 and located at the p35.3, is overexpressed in a few types of human cancer ( 10 – 12 ).…”

Matrine regulates H2O2-induced oxidative stress through long non-coding RNA HOTAIR/miR-106b-5p axis via AKT and STAT3 pathways

“…Previous study has demonstrated that HOTAIR exerted promotion effect on cell growth and inhibition effect on cell apoptosis in endometrial carcinoma by suppressing PTEN to activate PI3K/AKT pathway [41]. In another research, Qi et al reported that the activation of PI3K/AKT pathway-mediated by HOTAIR exhibited improvement effects on diabetic cardiomyopathy through facilitating the viability of cardiomyocytes [42].…”

Identification of long noncoding RNA RP11-89K21.1 and RP11-357H14.17 as prognostic signature of endometrial carcinoma via integrated bioinformatics analysis

“…In recent years, a variety of lncRNAs have been identi ed to be essential for the initiation, progression and malignant behaviors of endometrial carcinoma [11]. High expression of MALAT1 [12], HOTAIR [13] and NEAT1 [14] were closely associated with the poor prognosis of EC and promoted the proliferation, metastasis and EMT of endometrial cancer cells. Other studies have shown that the expression of MEG3 [15] and FER1L4 [16] were decreased in EC, and high expression of MEG3 and FER1L4 inhibited the proliferation, migration and invasion of endometrial cancer cells.…”