RETRACTED ARTICLE: Upregulation of long non-coding RNA OGFRP1 facilitates endometrial cancer through regulating miR-124-3p/SIRT1 axis and activating PI3K/AKT/GSK-3β pathway

Abstract

We planned to investigate the possible influences of long non-coding RNA (opioid growth factor receptor pseudogene 1) OGFRP1 in endometrial cancer and its potential regulatory mechanism. We measured the level of OGFRP1 in endometrial cancer tissues and evaluated the influences of OGFRP1 dysregulation on the tumour cell biological processes of endometrial cancer cells. Further, the regulatory relationships between OGFRP1 and miR-124-3p, between miR-124-3p and Sirtuin1 (SIRT1) were, respectively, investigated. The interaction between OGFRP1 dysregulation and activation of PI3K/AKT/ GSK-3b pathway was revealed by Western blotting. OGFRP1 was up-regulated in endometrial cancer tissues and cells. OGFRP1 suppression inhibited the malignant behaviour (inhibited cell viability, promoted cell apoptosis, and suppressed cell migration and invasion) of the Ishikawa cells via negatively regulating miR-124-3p. SIRT1 was a target gene of miR-124-3p, and miR-124-3p regulated tumour growth and metastasis by the downstream signal of SIRT1. Moreover, suppression of OGFRP1 restrained the activation of PI3K/AKT/GSK-3b signals in the Ishikawa cells via miR-124-3p/SIRT1 axis. Our experiments revealed that upregulation of OGFRP1 may enhance the progression of endometrial cancer by regulating miR-124-3p/SIRT1 axis and by activating PI3K/AKT/GSK-3b pathway. OGFRP1 may be of significance in illustrating the biology of endometrial cancer.

Pseudogene-Derived lncRNAs and Their miRNA Sponging Mechanism in Human Cancer

“…The expression level of OGFRP1 was significantly upregulated in endometrial cancer . Lv et al (2019) also experimentally confirmed that knockdown of OGFRP1 suppressed the malignant behaviors of endometrial cancer, including suppressed cell viability, enhanced cell apoptosis and inhibited cell migration and invasion. OCT4-pg5 was found to be aberrantly activated in endometrial cancer samples compared with benign endometrium samples, and increased expression of OCT4-pg5 enhanced proliferation by promoting OCT4/PI3K/AKT/CCND1 signaling (Bai et al, 2015).…”

MiR-629-3p-induced downregulation of SFTPC promotes cell proliferation and predicts poor survival in lung adenocarcinoma

“…Numerous studies have shown that microRNAs play a crucial part in regulating cancer cell apoptosis, proliferation, invasion, growth, and metastasis [23][24][25][26][27]. Therefore, we made a further exploration of whether SFTPC downregulation in lung cancer was mediated by microRNAs.…”

“…MiR-629-3p was upregulated in LUAD and a potential negative regulator to SFTPC MicroRNAs, a type of endogenous small molecule non-coding single-stranded RNAs, display a repressive effect on target gene expression or mRNA degradation [23,24]. Mountains of evidence show that microRNAs play crucial parts in regulating malignant cell apoptosis, proliferation, invasion, growth and metastasis [23][24][25][26][27]. Herein, we explored whether SFTPC expression was modulated by microRNAs in lung cancer.…”

“…MicroRNAs (miRNAs) are a type of endogenous small molecule non-coding single-stranded RNAs composed of 21-24 nucleotides and display a repressive effect on target gene expression through post-transcriptional suppression and mRNA degradation [23,24]. A large number of studies have shown that miRNAs play a crucial part in regulating tumour progression, including malignant cell apoptosis, proliferation, invasion, growth, and metastasis [23][24][25][26][27]. Therefore, by combining bioinformatics analysis and experimental validation of molecular biology we made a further exploration of whether SFTPC expression was regulated by microRNAs in lung cancer.…”

Retracted Article: MicroRNA-1271 modulates hepatitis B virus replication, cell proliferation and apoptosis in hepatitis B virus-related hepatocellular carcinoma by targeting SIRT1

“…33 On the contrary, SIRT1 was proved to promote tumor development in breast cancer and endometrial cancer. 34,35 Alves-Fernandes et al suggested that the contradictory role of SIRT1 might due to the different cell type and SIRT1 localization. 36 A previous study revealed that SIRT1 promoted HBV replication in hepatocytes.…”