lncRNA RHPN1‐AS1 promotes the progression of endometrial cancer through the activation of ERK/MAPK pathway

• Published in: The journal of obstetrics and gynaecology research Vol. 47; no. 2; pp. 533 - 543
• Main Authors: Zhang, Xian‐juan, Qi, Guang‐tao, Zhang, Xiao‐min, Wang, Li, Li, Fang‐fang
• Format: Journal Article
• Language: English
• Published: Kyoto, Japan John Wiley & Sons Australia, Ltd 01.02.2021; Wiley Subscription Services, Inc
• Subjects: Antisense RNA; Apoptosis; Bax protein; Caspase; Cell cycle; Cell Line, Tumor; Cell migration; Cell Proliferation; Cholecystokinin; Endometrial cancer; Endometrial Neoplasms - genetics; Endometrium; ERK/MAPK pathway; Extracellular signal-regulated kinase; Female; Flow cytometry; Gene Expression Regulation, Neoplastic; Humans; Immunofluorescence; Lymph nodes; MAP kinase; MAP Kinase Signaling System; Metastases; metastasis; Molecular modelling; Phosphorylation; Polymerase chain reaction; proliferation; RHPN1‐AS; Ribonucleic acid; RNA; RNA, Long Noncoding - genetics; RNA, Long Noncoding - metabolism; RNA-directed DNA polymerase; Wound healing; ERK/MAPK pathway; endometrial cancer; apoptosis; RHPN1-AS; proliferation; metastasis
• ISSN: 1341-8076; 1447-0756
• DOI: 10.1111/jog.14548

Aim This study aimed to investigate the function of long noncoding RNA RHPN1 antisense RNA 1 (lncRNA RHPN1‐AS1) in the progression of endometrial cancer (EC) and its underlying molecular mechanisms. Methods The RHPN1‐AS1 expression was measured by quantitative reverse transcriptase‐polymerase chain reaction (qRT‐PCR) in EC tissues and cells. The cell clones, proliferation, cell cycle, apoptosis, migration and invasion in Ishikawa and HEC‐1A cells were respectively measured by colony formation assay, cell counting kit‐8 assay (CCK‐8) assay, flow cytometry, wound healing assay and transwell assay. In addition, the protein expressions in Ishikawa and HEC‐1A cells were measured using western blot and Immunofluorescence assay. Results Our data showed the RHPN1‐AS1 expression was significantly upregulated in both EC tissues and cells. The expression of RHPN1‐AS1 was significantly correlated with FIGO stage, histological grade, and lymph node metastasis. Additionally, silencing RHPN1‐AS1 could inhibit proliferation, cell cycle progression, migration and invasion, and also promote apoptosis in Ishikawa and HEC‐1A cells. Moreover, silencing RHPN1‐AS1 could markedly elevate the expressions of caspase‐3 and Bax, but reduce the Bcl‐2 expression in Ishikawa and HEC‐1A cells. We also found that silencing RHPN1‐AS1 could significantly inhibit the phosphorylation of MEK and ERK in Ishikawa and HEC‐1A cells. After U0126 pretreatment, the inhibition effect of silencing RHPN1‐AS1 on the phosphorylation of MEK and ERK was strengthened. Conclusion Our study demonstrated that RHPN1‐AS1 could facilitate cell proliferation, migration and invasion, as well as inhibit apoptosis via activating ERK/MAPK pathway in EC.