MiR-3174 promotes proliferation and inhibits apoptosis by targeting FOXO1 in hepatocellular carcinoma

Wang, Qingyuan; Yang, Xiao; Zhou, Xiao; Wu, Bin; Zhang, Deming; Jia, Wenbo; Chu, Jian; Wang, Jinyi; Wu, Junli; Kong, Lianbao

doi:10.1016/j.bbrc.2020.03.152

Cited by 29 publications

(29 citation statements)

References 21 publications

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“…However, cancerous cells usually reduce the expression level of FOXO1 to promote the cell proliferation and inhibit the cell apoptosis. 42,43 In this study, we also observed the significant downregulation of FOXO1 in EC cells. Furthermore, we proved that the absence of FOXO1 was responsible for the reduction of cisplatin sensitivity to EC.…”

Section: Discussionsupporting

confidence: 68%

<p>Knockdown of miR-183 Enhances the Cisplatin-Induced Apoptosis in Esophageal Cancer Through Increase of FOXO1 Expression</p>

Chen

Zheng

Xue

et al. 2020

OTT

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Background: As an important member of platinum-based chemotherapeutic drugs, cisplatin is effective and is commonly used in the treatment of esophageal cancer. However, repeated use of cisplatin usually causes severe side-effects on patients. Novel approaches should be explored to increase the sensitivity of cancer cells to cisplatin. Methods: The expression level of miR-183 in esophageal cancer tissues and cell lines was measured by quantitative reverse transcriptase real-time PCR (qRT-PCR). The sensitivity of EC cell lines to cisplatin was evaluated by CCK-8 assay and flow cytometry. Luciferase reporter assay was used to confirm the association between miR-183 and FOXO1. The apoptosis pathway of EC cells was tested by Western blot assay. Results: The expression level of miR-183 was increased in esophageal cancer patients' tumor tissues and esophageal cancer cell lines. However, knockdown of miR-183 was found to enhance the effect of cisplatin on inducing the apoptotic cell death of esophageal cancer cells. In the mechanism research, we proved that FOXO1 was the target of miR-183 in esophageal cancer cells. Inhibition of miR-183 increased the expression of FOXO1 to promote the expression of Bim and Noxa. As Bim and Noxa acted as key pro-apoptotic proteins in mitochondrial apoptosis, inhibition of miR-183 enhanced the cisplatin-induced apoptosis pathway in esophageal cancer. Conclusion: Knockdown of miR-183 enhanced the cisplatin-induced apoptosis in esophageal cancer through an increase of FOXO1 expression.

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Section: Discussionsupporting

confidence: 68%

<p>Knockdown of miR-183 Enhances the Cisplatin-Induced Apoptosis in Esophageal Cancer Through Increase of FOXO1 Expression</p>

Chen

Zheng

Xue

et al. 2020

OTT

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“…Therefore, LINC02499 may be a useful predictive biomarker in the diagnosis and prognosis of HCC (37). Wang et al found that up-regulation of miR-3174 inhibited cell apoptosis and promote cell proliferation in HCC by down-regulating the expression of FOXO1, suggesting that miR-3174 may be a new therapeutic candidate for HCC patients (38). However, although some prognostic biomarkers of HCC have been identified, the results of studies so far have been inconsistent; moreover, an analysis at multiple omics levels has yet to be performed.…”

Section: Discussionmentioning

confidence: 99%

An aberrant DNA methylation signature for predicting hepatocellular carcinoma

Zhang

et al. 2020

Ann Transl Med

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Background: By the time they are clinically diagnosed, patients with hepatocellular carcinoma (HCC) are often at the advanced stage. DNA methylation has become a useful predictor of prognosis for cancer patients. Research on DNA methylation as a biomarker for assessing the risk of occurrence in HCC patients is limited. The purpose of this study was to develop an efficient methylation site model for predicting survival in patients with HCC.Methods: DNA methylation and gene expression profile data were extracted from The Cancer Genome Atlas (TCGA) database. Markers of DNA-methylated site in two subsets (the training subset and the test subset) were identified using a random survival forest algorithm and Cox proportional hazards regression.Then, Gene Ontology annotations were applied to investigate the functions of DNA methylation signatures.Results: A total of 37 hub genes containing 713 methylated sites were identified among the differentially methylated genes (DMGs) and differentially expressed genes (DEGs). Finally, seven methylation sites (cg12824782, cg24871714, cg18683774, cg22796509, cg19450025, cg10474350, and cg06511917) were identified. In the training group and the test group, the area under the curve predicting the survival of patients with HCC was 0.750 and 0.742, respectively. The seven methylation sites signature could be used to divide the patients in the training group into high-and low-risk subgroups [overall survival (OS): 2.81 vs. 2.11 years; log-rank test, P<0.05]. Then, the prediction ability of the model was validated in the test dataset through risk stratification (OS: 2.04 vs. 2.88 years; log-rank test, P<0.05). Functional analysis demonstrated that these signature genes were related to the activity of DNA-binding transcription activator, RNA polymerase II distal enhancer sequence-specific DNA binding, and enhancer sequence-specific DNA binding. Conclusions:The results of this study showed that the signature is useful for predicting the survival of HCC patients and thus, can facilitate treatment-related decision-making.

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“…miRNA widely present in eukaryotes plays an important regulatory role in life processes like cell proliferation, migration, invasion, which is a potential molecular target for tumor therapy (14). miR-3174 is a newly discovered miRNA with up-regulated expression in tumors of liver cancer (15), stomach cancer (16), etc. Downregulation of miR-3174 expression can inhibit the proliferation of tumor cells, induce apoptosis of tumor cells, and delay tumor development.…”

Section: Discussionmentioning

confidence: 99%

Cisatracurium inhibits the proliferation, migration and invasion of breast cancer cells by regulating the expression of miR-3174

Yang

2020

Cell Mol Biol (Noisy-le-grand)

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Breast cancer is a type of cancer that begins in the breast tissue. Being a woman is the most important factor in the risk of breast cancer. Although men also get the cancer, women are much more likely to get it. This experiment was founded to investigate the effect and mechanism of Cisatracurium on breast cancer cell proliferation, migration and invasion. Breast cancer cells MDA-MB-231 were cultured in vitro. MDA-MB-231 cells were treated with cisatracurium of different concentrations for 48 h. CCK-8method detected cell proliferation, Transwell detected cell migration and invasion, Western Blot method detected the expression levels of CyclinD1, p21, MMP-2andMMP-9protein in cells, RT-qPCR) detected the expression level of miR-3174in cells. After miR-3174 inhibitor was transfected into MDA-MB-231 in order to down-regulate the expression of miR-3174, the same methods as above were used to observe the effect of the down-regulating miR-3174 expression on MDA-MB-231 cell proliferation, migration and invasion as well as the expression levels of CyclinD1, p21, MMP -2 andMMP-9 protein. After different concentrations of Cisatracurium acted on MDA-MB-231 cells, the cell inhibition rate and p21 protein expression were significantly increased (p<0.05), the number of cell migration and invasion and the expression levels of CyclinD1, MMP-2 and MMP-9 were significantly reduced (p<0.05), and the expression of miR-3174 in cells was significantly reduced (p<0.05). After down-regulating the expression of miR-3174, the cell inhibition rate and p21 protein expression were significantly increased (p<0.05), the number of cell migration and invasion and the expression levels of CyclinD1, MMP-2 and MMP-9 were significantly reduced (p<0.05). Up-regulating miR-3174 expression could reverse the effect of Cisatracurium on the proliferation, migration and invasion of MDA-MB-231 cells. Cisatracurium can inhibit the proliferation, migration and invasion of breast cancer MDA-MB-231 cells, and its mechanism is related to the down-regulation of miR-3174 expression in cells.

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MiR-3174 promotes proliferation and inhibits apoptosis by targeting FOXO1 in hepatocellular carcinoma

Cited by 29 publications

References 21 publications

<p>Knockdown of miR-183 Enhances the Cisplatin-Induced Apoptosis in Esophageal Cancer Through Increase of FOXO1 Expression</p>

<p>Knockdown of miR-183 Enhances the Cisplatin-Induced Apoptosis in Esophageal Cancer Through Increase of FOXO1 Expression</p>

An aberrant DNA methylation signature for predicting hepatocellular carcinoma

Cisatracurium inhibits the proliferation, migration and invasion of breast cancer cells by regulating the expression of miR-3174

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