MiR-495-3p facilitates colon cancer cell proliferation via Wnt/β-catenin signaling pathway by restraining Wnt inhibitory factor

Lin, Lin; Tong, Gangling; Li, Meixiang; Liu, Aixue; Wang, Senming

doi:10.4314/tjpr.v16i9.10

Cited by 5 publications

(4 citation statements)

References 24 publications

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“…For example, miR-495-3p is sponged by lncRNA NEAT1 to regulate STAT3 expression, resulting in alleviation of septicemia-related inflammatory response (19). Moreover, it is worth noting that miR-495-3p serves as an inhibitory regulator in CRC (20). However, the relationship between LUNAR1 and miR-495-3p, and the specific mechanisms involved remain unclear.…”

Section: Introductionmentioning

confidence: 99%

lncRNA LUNAR1 accelerates colorectal cancer progression by targeting the miR‑495‑3p/MYCBP axis

Qian

Garg

et al. 2020

Int J Oncol

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Colorectal cancer (CRC) is a tumor type characterized by high patient morbidity and mortality. It has been reported that long non-coding (lncRNA) LUNAR1 (LUNAR1) participates in the regulation of tumor progression, such as diffuse large B-cell lymphoma. However, its role and underlying mechanisms in CRC progression have not been elucidated. The present study was designed to investigate the underlying mechanisms by which LUNAR1 regulates CRC progression. RT-qPCR and Pearson's correlation analysis revealed that LUNAR1 was highly expressed and was negatively associated with the overall survival of CRC patients. Moreover, CCK-8, clone formation, wound-healing migration, Transwell chamber and FACs assay analyses showed that LUNAR1 knockdown inhibited CRC cell proliferation, migration and invasion, while accelerating cell apoptosis. Additionally, LUNAR1 was found to function as a sponge of miR-495-3p, which was predicted by TargetScan and confirmed by luciferase reporter assay. Furthermore, functional studies indicated that miR-495-3p overexpression inhibited CRC cell proliferation, migration and invasion, while accelerating cell apoptosis. In addition, bioinformatics and luciferase reporter assays showed that miR-495-3p was found to negatively target Myc binding protein (MYCBP), and functional research showed that LUNAR1 accelerated CRC progression via the miR-495-3p/MYCBP axis. In conclusion, LUNAR1 accelerates CRC progression via the miR-495-3p/MYCBP axis, indicating that LUNAR1 may serve as a prognostic biomarker for CRC patients.

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Section: Introductionmentioning

confidence: 99%

lncRNA LUNAR1 accelerates colorectal cancer progression by targeting the miR‑495‑3p/MYCBP axis

Qian

Garg

et al. 2020

Int J Oncol

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“…Several studies showed that miR-495-3p inhibits the progression of prostate cancer, colorectal cancer and melanoma [6,20,21]. In contrast, recent study provided important evidence about an oncogenic role of miR-495-3p in colon cancer [7].…”

Section: Discussionmentioning

confidence: 99%

“…Li et al showed that miR-495-3p is downregulated in prostate cancer and regulates migration and invasion in prostate cancer cells by targeting AKT and mTOR transcripts [6]. In contrast, Lin et al analysis revealed that miR-495-3p expression level is elevated in colon tumors and confirmed an oncogenic role for this miRNA exerted by targeting the WIF1 gene, a Wnt/β-catenin signaling pathway inhibitor [7]. The various roles of miR-495 in cancer progression have been reviewed recently by Chen et al [4].…”

Section: Introductionmentioning

confidence: 99%

Downregulated miR-495-3p in colorectal cancer targets TGFβR1, TGFβR2, SMAD4 and BUB1 genes and induces cell cycle arrest

Soltani

Kabiri

Medlej

et al. 2019

Preprint

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• Background: Hsa-miR-495 (miR-495) has been extensively investigated in cancer initiation and progression. On the other hand, our bioinformatics analysis suggested that miR-495 exert its effects through targeting of TGFβ signaling components. • Methods & Results: In order to investigate such effect, miR-495 precursor was overexpressed in HEK293T and HCT116 cells, that it was followed by downregulation of TGFβR1, TGFβR2, SMAD4 and BUB1 putative target genes, detected by RT-qPCR. Also, luciferase assay supported direct interaction of miR-495 with 3’UTR sequences of TGFβR1, TGFβR2, SMAD4 and BUB1 genes. Furthermore, a negative correlation of expression between miR-495-3p and these target genes was deduced in a set of colorectal and breast cancer cell lines. Then, flow cytometry analysis showed that the overexpression of miR-495 in HCT116 and HEK293T resulted in an arrest at the G1 phase. Consistently, western blotting analysis showed a significant reduction of the Cyclin D1 protein in the cells overexpressing miR-495, pointing to downregulation of TGFβ signaling pathway and cell cycle arrest. Finally, microarray data analysis showed that miR-495-3p is significantly downregulated in colorectal tumors, compared to the normal pairs. • Conclusions: Overall, results of current study introduced miR-495-3p as a cell cycle progression suppressor, which negatively regulates TGFβR1, TGFβR2, SMAD4 and BUB1 genes. This finding suggests miR-495-3p as a tumor suppressor candidate for further evaluation.

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“…In the study conducted byLi et al (2016), the unusually high expression of miR-665 was also observed in both heart and plasma during heart failure, and the important role miR-665 played in discriminating patients from controls and affecting LVEF had been reported. In addition, we made observations of impaired cardiac function and promoted cell apoptosis when miR-665 had become upregulated.According to a recent study, overexpressing miR-665 was reported to have inhibited the proliferation, migration, and invasion of the vascular smooth muscle cells, with downregulating miR-665 capable of promoting those processes (K Li, Pan, Wang, Liu, & Wang, 2017)…”

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confidence: 99%

microRNA‐665 silencing improves cardiac function in rats with heart failure through activation of the cAMP signaling pathway

Lin

Feng

2019

Journal Cellular Physiology

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Heart failure (HF) is a disease with high mortality and morbidity rate. Previous studies have shown that microRNAs (miRNAs) may be implicated in the pathogenesis of HF, potentially being able to improve the cardiac function in an HF rat model. The present study was designed to define the role of miR‐665 in the cardiac function of the HF rats. Following the establishm;ent of the rat models of HF, the functional role miR‐665 in HF was determined using an ectopic expression and knockdown experiments. The cardiac function was evaluated with the determination of ventricular mass index and hemodynamic parameters. Terminal deoxynucleotidyl transferase dUTP nick end labeling staining was performed, with the apoptosis of cardiac cells detected in the process. The expression of miR‐665, glucagon‐like peptide 1 receptor (GLP1R), cyclic adenosine monophosphate (cAMP) signaling pathway‐related, and apoptosis‐related genes was examined. Enzyme‐linked immunosorbent assay was conducted to determine the levels of inflammation‐related genes. Initially, the upregulation of miR‐665, downregulation of GLP1R, and inactivation of cAMP signaling pathway were observed in HF rats. GLP1R was a target of miR‐665. Forced expression of miR‐665 promoted cell apoptosis and inhibited GLP1R and the cAMP signaling pathway. In addition, miR‐665 overexpression has been known to impair cardiac function, promote inflammatory response while elevating malondialdehyde and superoxide dismutase levels, and decreasing mitochondrial respiratory chain enzyme activities. Furthermore, we also observed that the effects of miR‐665 inhibition had been reversed when the cAMP signaling pathway was also inhibited. This study demonstrates that miR‐665 inhibition can stabilize the cardiac function of HF rats via the cAMP signaling pathway via upregulation of the GLP1R.

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MiR-495-3p facilitates colon cancer cell proliferation via Wnt/β-catenin signaling pathway by restraining Wnt inhibitory factor

Cited by 5 publications

References 24 publications

lncRNA LUNAR1 accelerates colorectal cancer progression by targeting the miR‑495‑3p/MYCBP axis

lncRNA LUNAR1 accelerates colorectal cancer progression by targeting the miR‑495‑3p/MYCBP axis

Downregulated miR-495-3p in colorectal cancer targets TGFβR1, TGFβR2, SMAD4 and BUB1 genes and induces cell cycle arrest

microRNA‐665 silencing improves cardiac function in rats with heart failure through activation of the cAMP signaling pathway

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