The miR-124-p63 feedback loop modulates colorectal cancer growth

Liu, Kuijie; Yao, Hongliang; Lei, Sanlin; Li, Xiong; Qi, Haiyun; Ke, Qing; Liu, Jiqiang; Wang, Peng; Zhao, Hua

doi:10.18632/oncotarget.16248

Cited by 25 publications

(22 citation statements)

References 53 publications

(69 reference statements)

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“…As described in our research, we showed that noncoding RNAs were involved in breast cancer metastasis and miR-124 inhibited cell proliferation in breast cancer [16][17][18]. Consistent with our findings, miR-124 was decreased in colorectal tissue samples and was correlated with adverse clinical indicators and poor patient survival time [19][20][21]. Downregulation of plasma miR-124 expression was a predictive biomarker for prognosis of glioma [10,22].…”

Section: Discussionsupporting

confidence: 89%

Evaluation of the Role of hsa-mir-124 in Predicting Clinical Outcome in Breast Invasive Carcinoma Based on Bioinformatics Analysis

Feng

Zhang

Sun

et al. 2020

BioMed Research International

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Purpose. Breast invasive carcinoma (BRCA) is the most common malignant tumor. MiR-124 plays a tumor-suppressive role in human cancer. However, the clinical significance of miR-124 in BRCA remains unclear. The aim of this study was to evaluate the association of hsa-mir-124 expression and the clinicopathological characteristics in BRCA using database analysis. Methods. The clinical data and expression profiles of hsa-mir-124 were obtained from the cancer genome atlas for BRCA (TCGA_BRCA). Then, the prognostic value of hsa-mir-124 in BRCA was investigated using the Cox Regression test, and the association of hsa-mir-124 and pathology TNM stages and pathologic stages were measured by the Kruskal–Wallis test and Wilcox. test. In addition, the association of hsa-mir-124 and tumor molecular phenotypes was performed using the Chi-Square test. Results. We found that the overall survival of patients with high expression of hsa-mir-124-1 and hsa-mir-124-2 was better than that of patients with low expression of hsa-mir-124-1 and hsa-mir-124-2. And the expression of hsa-mir-124-1, hsa-mir-124-2, and hsa-mir-124-3 was mainly enriched in T1/T2 stages, NO/N1 stages, and M0 stages. Then, the expression of hsa-mir-124-1, hsa-mir-124-2, and hsa-mir-124-3 was negatively associated with tumor lymph node metastasis. Moreover, the expression of hsa-mir-124 was associated with tumor molecular phenotype in breast invasive carcinoma. Conclusion. Our findings indicated that hsa-mir-124 expressions were associated with overall survival, TNM stages, pathologic characteristics, and tumor molecular phenotype in BRCA via TCGA_BRCA database, providing a new biomarker and a potential therapeutic target for BRCA patients.

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Section: Discussionsupporting

confidence: 89%

Evaluation of the Role of hsa-mir-124 in Predicting Clinical Outcome in Breast Invasive Carcinoma Based on Bioinformatics Analysis

Feng

Zhang

Sun

et al. 2020

BioMed Research International

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“…MicroRNAs (miRNAs) are non-coding RNA molecules with a length of 18-22 nt. They regulate gene expression through targeted binding of the 3' untranslated region (3'UTR) terminal of mRNA molecules (4). In recent years, numerous scholars have confirmed that miRNA molecules in tumor tissue are novel markers for clinical tumor diagnosis.…”

Section: Introductionmentioning

confidence: 99%

Upregulation of miR-542-3p inhibits the growth and invasion of human colon cancer cells through PI3K/AKT/survivin signaling

et al. 2017

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The present study was designed to assess the expression of microRNA-542-3p (miR-542-3p) in human colon cancer and investigate the possible molecular mechanisms underlying the effect of miR-542-3p on the growth and invasion of colon cancer cells. We found that miR-542-3p expression was downregulated in colon cancer patient tissues, compared with that observed in the control group. Silencing of miR‑542-3p expression significantly promoted cell viability and inhibited apoptosis. In addition, overexpression of miR-542-3p significantly reduced cell viability and promoted apoptosis in colon cancer cells. Meanwhile, silencing of miR-542-3p expression significantly suppressed PI3K and p-AKT and survivin protein expression, while overexpression of miR-542-3p significantly induced PI3K and p-AKT and survivin protein expression in colon cancer cells. PI3K inhibitor (LY294002) or survivin inhibitor (YM155) suppressed PI3K/AKT/survivin signaling and increased the anticancer effects of miR-542-3p on the apoptosis in colon cancer. The present study demonstrated that upregulation of miR-542-3p inhibited the growth and invasion of colon cancer cells through PI3K/AKT/survivin signaling, highlighting a novel therapeutic approach for the treatment of colon cancer.

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“…Also, retinoic orphan receptor-γ (RORγ) and signal transducer and activator of transcription 3 (STAT3)are the transcription factors responsible for Th17 differentiation andstabilization.Gerogios et al demonstrated that miR-124 could promote the children UC and pathogenesis by regulating the expression and phosphorylation of STAT3, but special cell type was not involved [14]. The previous study also demonstrated that miR-124 depression was related to carcinogenesis, and development by targeting different gene [23,24,25].These observations suggested that miR-124 played an key role in colitis and sporadic colon cancer.In our present study, we focused on the miR-124 function in Th17 cell and found that miR-124 could inhibit the polarization of Th17 cell and promote the transition of Th17 to treg in colitis and colitis related colon cancer by targeting stat3 gene.These results are consistent with downregulation of miR-124 developingintestinal failure with M1 macrophage phenotype by targeting stat3 and acetylcholinesterase (AChE). We believe that in the absence of miR-124 signaling cascade, the presence of intestinal commensal bacteria will drive intestinal CD4 + T helper cells toward Th17 cell polarization, resulting in a hyper-in ammatory response with associated tissue damage and pathogenesis.…”

Section: Discussionmentioning

confidence: 97%

STAT3-mediated TH17 cell Differentiation was Related to the Carcinogenesis of Colitis Related Cancer

Lin¹,

Liu²,

Wen³

et al. 2020

Preprint

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Background: Inflammation often induces regeneration to repair the tissue damage. However, chronic inflammation can transform temporary hyperplasia into a fertile ground for tumorigenesis. Here, we demonstrate that the miR-124 acts as a safeguard to inhibit the pro-inflammatory production and reparative regeneration.Methods: The expression levels of miR-124 and IL-17, IFN-γ were analyzed by quantitative real-time polymerase chain reaction (qRT-PCR). TH17 or TH1 cells were detected by flow cytometer, respectively. the binding of STAT3 to the promoter region of IL-17 gene was analyzed by Chip assay . miR-124 binding to the 3’UTR of STAT3 gene was detected by reported plasmid construction and luciferase assay. Furthermore, DSS-induced colitis mice model and T cell transfer model were used to confirm the function of miR-124 in vivo. The related gene expression was analyzed by ELISA and western blot experiments.Results: The results indicated that miR-124a deficiency leads to colon tumorigenesis after Citrobacter rodentium infection and AOM/DSS induced colon cancer murine model. In molecular mechanism, miR-124 targets STAT3 to suppress T helper 17 (TH17) cell differentiation and expansion, and keep TH17 polarization in colonic microenvironment.Conclusions: Our study highlights highlight the potential role of miR-124 in the control of immune responses and pathogenesis of inflammatory diseases.

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The miR-124-p63 feedback loop modulates colorectal cancer growth

Cited by 25 publications

References 53 publications

Evaluation of the Role of hsa-mir-124 in Predicting Clinical Outcome in Breast Invasive Carcinoma Based on Bioinformatics Analysis

Evaluation of the Role of hsa-mir-124 in Predicting Clinical Outcome in Breast Invasive Carcinoma Based on Bioinformatics Analysis

Upregulation of miR-542-3p inhibits the growth and invasion of human colon cancer cells through PI3K/AKT/survivin signaling

STAT3-mediated TH17 cell Differentiation was Related to the Carcinogenesis of Colitis Related Cancer

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