lncRNA RHPN1-AS1 Serves as a Sponge for miR-3133 Modulating the Cell Proliferation of Retinoblastoma through JAK2

Li, Zhao‐Na; Ge, Mingtao; Cao, Liu; Yuan, Zhongfang

doi:10.1155/2020/3502981

Cited by 7 publications

(7 citation statements)

References 28 publications

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“…To date, the role of miR-3133 in cancer has been poorly investigated, except in retinoblastoma and clear cell renal cell carcinoma. 45,46 In line with the above findings, our data indicate that miR-3133 plays a tumour-suppressive role in GIC. Previous studies have shown that miR-3133 is expressed at low levels in tumour tissues, but the mechanism of its downregulation remained unclear.…”

Section: Discussionsupporting

confidence: 89%

“…In this study, we found that a newly discovered miRNA, named miR‐3133, is involved in the proliferation of GIC cells. To date, the role of miR‐3133 in cancer has been poorly investigated, except in retinoblastoma and clear cell renal cell carcinoma 45,46 . In line with the above findings, our data indicate that miR‐3133 plays a tumour‐suppressive role in GIC.…”

Section: Discussionsupporting

confidence: 87%

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miR‐3133 inhibits gastrointestinal cancer progression through activation of Hippo and p53 signalling pathways via multi‐targets

Zhou

Guo

Liao

et al. 2023

J Cellular Molecular Medi

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BackgroundMalignant cell growth and chemoresistance, the main obstacles in treating gastrointestinal cancer (GIC), rely on the Hippo and p53 signalling pathways. However, the upstream regulatory mechanisms of these pathways remain complex and poorly understood.MethodsImmunohistochemistry (IHC), western blot and RT‐qPCR were used to analyse the expression of RNF146, miR‐3133 and key components of Hippo and p53 pathway. CCK‐8, colony formation, drug sensitivity assays and murine xenograft models were used to investigate the effect of RNF146 and miR‐3133 in GIC. Further exploration of the upstream regulatory mechanism was performed using bioinformatics analysis, dual‐luciferase reporter gene, immunoprecipitation assays and bisulfite sequencing PCR (BSP).ResultsClinical samples, in vitro and in vivo experiments demonstrated that RNF146 exerts oncogenic effects in GIC by regulating the Hippo pathway. Bioinformatics analysis identified a novel miRNA, miR‐3133, as an upstream regulatory factor of RNF146. fluorescence in situ hybridization and RT‐qPCR assays revealed that miR‐3133 was less expressed in gastrointestinal tumour tissues and was associated with adverse pathological features. Functional assays and animal models showed that miR‐3133 promoted the proliferation and chemotherapy sensitivity of GIC cells. miR‐3133 affected YAP1 protein expression by targeting RNF146, AGK and CUL4A, thus activating the Hippo pathway. miR‐3133 inhibited p53 protein degradation and extended p53's half‐life by targeting USP15, SPIN1. BSP experiments confirmed that miR‐3133 promoter methylation is an important reason for its low expression.ConclusionmiR‐3133 inhibits GIC progression by activating the Hippo and p53 signalling pathways via multi‐targets, including RNF146, thereby providing prognostic factors and valuable potential therapeutic targets for GIC.

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Section: Discussionsupporting

confidence: 89%

Section: Discussionsupporting

confidence: 87%

miR‐3133 inhibits gastrointestinal cancer progression through activation of Hippo and p53 signalling pathways via multi‐targets

Zhou

Guo

Liao

et al. 2023

J Cellular Molecular Medi

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“…In retinoblastoma (RB) cells, RHPN1‐AS1 was upregulated. Silencing RHPN1‐AS1 inhibited the activity of RB cells and promoted apoptosis 31 . In our study, we found that expression of RHPN1‐AS1 markedly upregulated in PCa tissues and cells, silencing RHPN1‐AS1 inhibited proliferation and invasion, and induced apoptosis in PCa cells.…”

Section: Discussionsupporting

confidence: 50%

“…Overexpression of RHPN1-AS1 promoted proliferation and metastasis of EOC cells, knockdown of RHPN1-AS1 significantly inhibited the proliferation, migration and invasion of ovarian cancer cells. 11,30 In retinoblastoma (RB) cells, RHPN1-AS1 was 31 In our study, we found that expression of RHPN1-AS1 markedly upregulated in PCa tissues and cells, silencing RHPN1-AS1 inhibited proliferation and invasion, and induced apoptosis in PCa cells. Moreover, we found that overexpression of miR-7-5p or silencing EGFR induced PCa cell apoptosis.…”

Section: Discussionmentioning

confidence: 68%

LncRNA RHPN1‐AS1 inhibition induces autophagy and apoptosis in prostate cancer cells via the miR‐7‐5p/EGFR/PI3K/AKT/mTOR signaling pathway

Ren

Zhang

et al. 2022

Environmental Toxicology

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lncRNA RHPN1-AS1 (RHPN1-AS1) has been con rmed to promote tumor progression in multiple cancers and is upregulated in prostate cancer (PCa), but whether it has an effect on PCa progression remains unclear. In this study, we found that PCa patients with high RHPN1-AS1 expression had a shorter survival time, and RHPN1-AS1 was signi cantly upregulated in PCa tissues and cells. Based on informatics analysis we predicted that miR-7-5p binds to 3'UTR of RHPN1-AS1 and epidermal growth factor receptor (EGFR) and veri ed it by luciferase reporter gene assay. Subsequently, we transfected PCa cells with RHPN1-AS1 overexpression vector (RHPN1-AS1), knockdown plasmids (sh-RHPN1-AS1) and/or miR-7-5p mimics or inhibitor and/or overexpression vector (EGFR) or small interfering RNA of EGFR (si-EGFR) or its control, and found that overexpression of RHPN1-AS1 inhibited miR-7-5p expression and promoted EGFR expression, silencing RHPN1-AS1 inhibited proliferation and invasion and induced G2/M arrest, apoptosis and autophagy in PCa cells. 3MA (an inhibitor of autophagy)-mediated autophagy inhibition attenuated RHPN1-AS1 inhibition-induced apoptosis. Overexpression miR-7-5p or silencing EGFR promoted LC3-I to LC3-II conversion, enhanced autophagy activity, induced cleaved-caspase-3 expression and apoptosis in PCa cells. Furthermore, we found that overexpression of RHPN1-AS1 promoted phosphorylation of phosphatidylinositol 3-kinase (PI3K), AKT and mTOR, inhibited LC3-I to LC3-II conversion and reduced apoptosis in PCa cells, while GSK2126458 (an inhibitor of PI3K) reversed the effect of RHPN1-AS1 on PCa cells. In summary, RHPN1-AS1 acted as a ceRNA of miR-7-5p to upregulate EGFR expression, silencing RHPN1-AS1 suppressed PCa tumor progression by inducing autophagy and apoptosis in PCa cells through the miR-7-5p/EGFR/PI3K/AKT/mTOR pathway.

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“…For instance, offsetting miR-3133-mediated JAK2/STAT3 inactivation aggravates RB. [35] Ribonucleotide reductase subunit M2 accelerates proliferation and EMT in RB through JAK2/STAT3. [36] As expected, this study revealed that SOCS3 was raised, and p-JAK2, p-STAT3 were decreased after miR-452-5p knockdown, while si-SOCS3 abolished these trends, implying that miR-452-5p might facilitate RB process through SOCS3/JAK2/STAT3.…”

Section: Interference With Mir-452-5p Represses Rb Tumor Growth Invas...mentioning

confidence: 99%

MiR‐452‐5p facilitates retinoblastoma cell growth and invasion via the SOCS3/JAK2/STAT3 pathway

Wu,

Huang,

Hong

et al. 2023

J Biochem & Molecular Tox

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Retinoblastoma (RB) is an intraocular tumor in children. Accumulated evidence confirms that microRNAs (miRNAs) exert critical functions in RB. This research aimed to investigate the miR‐452‐5p function in RB. MiR‐452‐5p expressions in RB were tested with quantitative real‐time polymerase chain reaction (PCR). MiR‐452‐5p functions in RB were evaluated via Cell Counting Kit‐8, 5‐Ethynyl‐2′‐deoxyuridine assay, flow cytometry, Western blot, and Transwell. MiR‐452‐5p mechanism in RB was assessed using bioinformatics software Starbase and dual‐luciferase reporter gene assay. Meanwhile, miR‐452‐5p function in RB in vivo was examined by constructing tumor xenografts in nude mice, immunohistochemistry, and Western blot assays. MiR‐452‐5p was overexpressed in RB tissues and cells, and miR‐452‐5p expression was positively correlated with RB clinicopathology including the Largest tumor base (mm) and Differentiation. Functionally, miR‐452‐5p knockdown restrained RB cell proliferation, invasion, epithelial–mesenchymal transition (EMT), and facilitated cell apoptosis. Mechanistically, suppressors of cytokine signaling (SOCS3) knockdown restored the inhibitory effects of miR‐452‐5p knockdown on RB cells. Meanwhile, in vivo studies further corroborated that miR‐452‐5p knockdown reduced RB tumor growth, EMT, and accelerated apoptosis in vivo. Also, miR‐452‐5p knockdown increased SOCS3 protein levels, and decreased phosphorylated Janus kinase 2/Janus kinase 2 (JAK2), phosphorylated signal transducer and activator of transcription 3/signal transducer and activator of transcription 3 (STAT3) in vivo. MiR‐452‐5p accelerated RB cell growth and invasion by SOCS3/JAK2/STAT3.

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lncRNA RHPN1-AS1 Serves as a Sponge for miR-3133 Modulating the Cell Proliferation of Retinoblastoma through JAK2

Cited by 7 publications

References 28 publications

miR‐3133 inhibits gastrointestinal cancer progression through activation of Hippo and p53 signalling pathways via multi‐targets

miR‐3133 inhibits gastrointestinal cancer progression through activation of Hippo and p53 signalling pathways via multi‐targets

LncRNA RHPN1‐AS1 inhibition induces autophagy and apoptosis in prostate cancer cells via the miR‐7‐5p/EGFR/PI3K/AKT/mTOR signaling pathway

MiR‐452‐5p facilitates retinoblastoma cell growth and invasion via the SOCS3/JAK2/STAT3 pathway

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