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.
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.