MiR-424-3p suppresses galectin-3 expression and sensitizes ovarian cancer cells to cisplatin

Bieg, Dominik; Sypniewski, Daniel; Nowak, Ewa; Bednarek, Ilona

doi:10.1007/s00404-018-4999-7

Cited by 36 publications

(24 citation statements)

References 27 publications

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“…Niu et al demonstrated that the expression of miR-509-3p was significantly downregulated in cisplatin-resistant ovarian cancer tissues, and that this miRNA can sensitize ovarian cancer cells to cisplatin by the downregulation of the expression of Golgi phosphoprotein-3 and wntless Wnt ligand secretion mediator 22 . Dominik et al revealed that miR-424-3p sensitizes ovarian cancer cells to cisplatin through decreases in the expression of galectin-3 23 . Since miRNAs do not require perfectly complementary target sites, a single miRNA regulates hundreds of genes, and a single oncogene is regulated by hundreds of miRNAs.…”

Section: Discussionmentioning

confidence: 99%

Paclitaxel exposure downregulates miR-522 expression and its downregulation induces paclitaxel resistance in ovarian cancer cells

Miyamoto

Sawada

Nakamura

et al. 2020

Sci Rep

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Paclitaxel resistance is a critical challenge in ovarian cancer treatment. This study aimed to identify microRNAs (miRNAs) that modulate paclitaxel resistance for use as potential therapeutic targets in such settings. Paclitaxel-resistant cell lines were established using two ovarian cancer cell lines: SKOV3ip1 and HeyA8. The evaluation of miRNA polymerase chain reaction (PCR) arrays indicated that the expression of miR-522-3p was downregulated in paclitaxel-resistant cells. The restoration of miR-522-3p sensitized the resistant cells to paclitaxel, and its downregulation desensitized the parental cells. Using PCR arrays, we focused on E2F2, with the luciferase reporter assay revealing that it was a direct target for miR-522-3p. The paclitaxel-resistant cells showed stronger E2F2 expression than the parental cells, while E2F2 inhibition sensitized the resistant cells to paclitaxel. Forced E2F2 expression in the parental cells led to the acquisition of paclitaxel resistance, while miR-522-3p inhibited E2F2 expression and was associated with retinoblastoma protein phosphorylation attenuation, which resulted in G0/G1 arrest. The effects of miR-522-3p and E2F2 in ovarian cancer were examined using public databases, revealing that low miR-522-3p expression and high E2F2 expression were associated with significantly poorer overall survival. In conclusion, miR-522-3p attenuated the degree of paclitaxel resistance in vitro through the downregulation of E2F2; miR-522-3p supplementation may be a therapeutic target for paclitaxel-resistant ovarian cancer.

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Section: Discussionmentioning

confidence: 99%

Paclitaxel exposure downregulates miR-522 expression and its downregulation induces paclitaxel resistance in ovarian cancer cells

Miyamoto

Sawada

Nakamura

et al. 2020

Sci Rep

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“…50 In our study, the expression of miR-424 in DDP resistant group was significantly decreased in compared with the DDP chemosensitive group, which was consistent with other research. 51,52 In present study, hub genes were screened by the plug-in CytoHubba, among the top 10 hubgenes in downregulation miRNA group, 8 of them were identified as the target genes of miRNA-424(CDC27, CDC23, RNF213, SMURF1, SMURF2, UBE4A, LMO7, WSB1), the hub gens were continued to be screened by Coremine Medical online database. Coremine Medical is a domainspecific search engine for medical information, which was based on a new search concept that offers the user domainspecific networks.…”

Section: Discussionmentioning

confidence: 99%

<p>MicroRNA-424 regulates cisplatin resistance of gastric cancer by targeting SMURF1 based on GEO database and primary validation in human gastric cancer tissues</p>

Lü¹,

Wu²,

Lu³

et al. 2019

OTT

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Purpose: Cisplatin (DDP) based chemotherapy regimens are widely used in advanced gastric cancer (GC). Drug resistance often limited the clinical benefits of cisplatin regimen. The mechanisms of cisplatin resistance have not been fully revealed. Therefore, further exploration of the relevant molecular mechanisms is urgently needed. Patients and methods: DDP resistance associated miRNA of GC microarray dataset GSE86195 was obtained from the National Center for Biotechnology Information (NCBI) GEO database, GEO2R was applied to compare the samples in two different groups under the same experimental conditions. |log 2 (Fold Change) | (log 2 (FC)) was selected as the criteria to screen the statistically significant DE-miRNAs. StarBaseV3.0 was used to predict the target genes of the DE-miRNAs. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses of target genes of DE-miRNAs were carried out using DAVID. The STRING database was applied to estimate the correlations between target genes. Analysis of hubgenes by coremine and The Human Protein Atlas (THPA). Initial expression validations of miR-424 and miR-491-5p, SMURF1 and BCL2L1 were carried out using clinical pathological specimens by RT-PCR. Results: A total of 13 Differential expression-miRNAs (DE-miRNAs) were identified in DDP chemoresistant cells, including 9 upregulated miRNAs and 4 downregulated miRNAs. SMURF1 and BCL2L1 were screened as the critical genes in DDP-resistant GC, which were regulated by miR-424 and miR-491-5p respectively. The results of validation of hub genes expression in GC tissues indicated that in DFS<1-year group, the expression of miR-424 decreased significantly, notably upregulated expression of SMURF1 was also detected. Conclusion: Our results implied that miR-424, as a tumor suppressor, could deregulate SMURF1 in DDP-resistant GC cells.

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“…Protein levels of GAL‐3 can be modulated by specific micro‐RNA molecules (miR) (Ramasamy et al, ). In this regard, a very recent elegant study has shown that miR‐424‐3p (known as miR‐322) can degrade GAL‐3 in SKOV3 without altering its mRNA transcription and rendered these tumor cells more sensitive to cisplatin‐induced cell death (Bieg et al, ). Similarly, but in lung cancerous cells, miR‐424‐3p inhibited cell migration, invasion, and proliferation and enhanced their sensitivity to cisplatin and paclitaxel (Zhang, Zeng, Zhao, & Liu, ).…”

Section: Discussionmentioning

confidence: 99%

“…Primers used to study mRNA levels of GAL‐3, and miR‐424‐3p (Acc. # NM_002306.3) were adopted from the study of Bieg, Sypniewski, Nowak, and Bednarek (). The primer pairs used to study mRNA of β‐actin (Acc.…”

Section: Methodsmentioning

confidence: 99%

The apoptotic effect of resveratrol in ovarian cancer cells is associated with downregulation of galectin‐3 and stimulating miR‐424‐3p transcription

et al. 2019

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This study investigated if the well‐reported anti‐tumor effects of resveratrol (RES) is mediated by modulation levels of galectin‐3 (GAL‐3), an anti‐apoptotic lectin that is highly overexpressed in ovarian cancer cells. SKOV3 and OVCAR‐3 OC cells were untreated or incubated with DMOS or increasing concentrations of RES (25, 50, 100 μM) for 72 hr. RES, in a dose‐dependent manner and in both cell lines, induced cell death and inhibited cell migration and invasion It also downregulated Bcl‐2 levels, increased cleaved caspase‐3, and GAL‐3 protein (but not mRNA) levels, suggesting increased breakdown. These effects were associated with reduced levels of p‐NF‐κB P65, p‐IKKα/β, and p‐Akt, major targets of Gal‐3. Further investigation showed that RES enhanced levels of miR‐424‐3p which is able to degrade GAL‐3. Conclusion: Findings of this study suggest that RES induced apoptosis in cancerous cells is associated with increased levels of miR‐424‐3p and reduced levels of GAL‐3. Practical applications This study highlights a possible mechanism by which RES could enhance cell death in OC cells and enhances their sensitivity to cisplatin. RES apoptotic effect and enhancement of OC cells to chemotherapy were associated with decreased abundance of GAL‐3, a common cell survival molecule that promotes tumorigenesis and increased transcription of miR‐424‐3p that has the ability to degrade cellular GAL‐3. These findings add a possible new mechanism by which RES acts and opens a window for further research to understand its mechanism of action.

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MiR-424-3p suppresses galectin-3 expression and sensitizes ovarian cancer cells to cisplatin

Cited by 36 publications

References 27 publications

Paclitaxel exposure downregulates miR-522 expression and its downregulation induces paclitaxel resistance in ovarian cancer cells

Paclitaxel exposure downregulates miR-522 expression and its downregulation induces paclitaxel resistance in ovarian cancer cells

<p>MicroRNA-424 regulates cisplatin resistance of gastric cancer by targeting SMURF1 based on GEO database and primary validation in human gastric cancer tissues</p>

The apoptotic effect of resveratrol in ovarian cancer cells is associated with downregulation of galectin‐3 and stimulating miR‐424‐3p transcription

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