Deregulation of miR-93 and miR-143 in human esophageal cancer

Ansari, Mohammad Hossein; Irani, Shiva; Edalat, Houri; Amin, Ruhul; Roushandeh, Amaneh Mohammadi

doi:10.1007/s13277-015-3987-9

Cited by 38 publications

(22 citation statements)

References 63 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In nasopharynx cancer, CCAT1 modulates paclitaxel sensitivity via the miR‐181a/CPEB2 axis . CCAT1 was also shown to act as an oncogene and promoted chemoresistance in docetaxel‐resistant lung adenocarcinoma cells . Furthermore, our results revealed that the expression of CCAT1 in ESCC cells is positively correlated with drug resistance, as we observed that higher CDDP sensitivity correlated with lower CCAT1 expression in several ESCC cell lines.…”

Section: Discussionsupporting

confidence: 62%

lncRNA CCAT1 is a biomarker for the proliferation and drug resistance of esophageal cancer via the miR‐143/PLK1/BUBR1 axis

Zhang

Tian

et al. 2019

Molecular Carcinogenesis

View full text Add to dashboard Cite

Recent evidence indicates that long noncoding RNA colon cancer‐associated transcript‐1 (lncRNA CCAT1) is abundantly expressed in esophageal cancer and is closely related to the occurrence, development, invasion, metastasis, and drug resistance of this disease. However, the role and molecular mechanisms of CCAT1 in the cell proliferation and chemoresistance of esophageal cancer are largely unknown. The correlation between CCAT1 expression and drug resistance to cisplatin (CDDP) in esophageal squamous cell carcinoma (ESCC) cells was analyzed using 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyl‐tetrazolium bromide (MTT) and quantitative real‐time polymerase chain reaction (qRT‐PCR) assays. CCAT1 knockdown and miR‐143 overexpression or inhibition were used to verify the effects on proliferation and drug resistance via MTT, western blotting, flow cytometry, and immunofluorescence assays. qRT‐PCR and western blotting were applied to detect the potential regulatory relationship among CCAT1, miR‐143, PLK1, and BUBR1. A xenograft tumor assay was performed to validate the role of CCAT1 in vivo. The expression of CCAT1 was positively correlated with drug resistance in several ESCC cell lines. CCAT1 knockdown and miR‐143 overexpression inhibited cell proliferation and CDDP drug resistance. Moreover, the downstream target of CCAT1 was found to be miR‐143, which can regulate the expression of PLK1 and BUBR1. In vivo assays showed that CCAT1 knockdown suppressed tumor growth and enhanced the sensitivity of tumors to CDDP in nude mice. Taken together, we discovered a novel mechanism by which CCAT1 promotes cell proliferation and enhances drug resistance by regulating the miR‐143/PLK1/BUBR1 signaling axis both in vitro and in vivo. Our findings further suggest that lncRNA CCAT1 may be a potential therapeutic target for overcoming chemoresistance in esophageal cancer.

show abstract

Section: Discussionsupporting

confidence: 62%

lncRNA CCAT1 is a biomarker for the proliferation and drug resistance of esophageal cancer via the miR‐143/PLK1/BUBR1 axis

Zhang

Tian

et al. 2019

Molecular Carcinogenesis

View full text Add to dashboard Cite

show abstract

“…MiR-93 acts as a tumor promoter and may also be used as a potential biomarker for esophageal squamous cell carcinoma (ESCC) [18, 19], which was in complete agreement with the current finding based on TCGA data.…”

Section: Discussionsupporting

confidence: 89%

Identification of molecular targets for esophageal carcinoma diagnosis using miRNA-seq and RNA-seq data from The Cancer Genome Atlas: a study of 187 cases

et al. 2017

View full text Add to dashboard Cite

Esophageal carcinoma (ESCA) is one of the most common malignancies worldwide, and its pathogenesis is complex. In this study, we identified differentially expressed miRNAs (DEMs) and genes (DEGs) of ESCA from The Cancer Genome Atlas (TCGA) database. The diagnostic values of DEMs were determined by receiver operating characteristic (ROC) analyses and validated based on data from Gene Expression Omnibus (GEO). The top five DEMs with the best diagnostic values were selected, and their potential targets were predicted by various in silico methods. These target genes were then identified among the DEGs from TCGA. Furthermore, the overlapping genes were subjected to protein-protein interaction (PPI) analysis, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses. The miRNA-transcription factor (TF) regulatory relations were determined using CircuitsDB and TransmiR. Finally, the regulatory networks of miRNA-TF and miRNA-gene were constructed and analyzed. A total of 136 DEMs and 3541 DEGs were identified in ESCA. The top five DEMs with the highest area under the receiver operating characteristic curve (AUC) values were miRNA-93 (0.953), miRNA-21 (0.928), miRNA-4746 (0.915), miRNA-196a-1 (0.906) and miRNA-196a-2 (0.906). The combined AUC of these five DEMs was 0.985. The KEGG analysis with 349 overlapping genes showed that the calcium signaling pathway and the neuroactive ligand-receptor interaction were the most relevant pathways. The regulatory networks of miRNA-TF and miRNA-gene, including 38 miRNA-TF and 560 miRNA-gene pairs, were successfully established. Our findings may provide new insights into the molecular mechanisms of ESCA pathogenesis. Future research will aim to explore the role of novel miRNAs in the pathogenesis and improve the early diagnosis of ESCA.

show abstract

“…For instance, the expression of miR-93 was found to be significantly increased in esophageal squamous cell carcinoma (12). Moreover, miR-93 can promote the transforming growth factor (TGF)-β-induced epithelial-to-mesenchymal transition through directly targeting neural precursor cell expressed developmentally downregulated gene 4-like in lung cancer cells (13).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-93 promotes cell proliferation by directly targeting P21 in osteosarcoma cells

2017

Experimental and Therapeutic Medicine

View full text Add to dashboard Cite

Abstract. MicroRNAs (miRNAs) are small, non-coding RNAs that are key regulators of gene expression by directly binding to the 3'-untranslated region of their target mRNAs, resulting in translational repression or degradation of mRNA. It has been demonstrated that miRNAs have key roles in a variety of human malignancies, including osteosarcoma. The present study aimed to assess the molecular mechanism of miR-93 in the regulation of osteosarcoma cell proliferation. Reverse-transcription quantitative PCR and western blot assays were used to examine mRNA and protein expression. An MTT assay and flow cytometry were performed to determine the cell proliferation and cell cycle distribution. A luciferase reporter assay was performed to confirm the direct targeting of cyclin-dependent kinase inhibitor 1A (CDKN1A), also known as P21, by miR-93, which was suggested by a bioinformatics analysis. The results showed that the expression of miR-93 was frequently and significantly increased in a total of 19 osteosarcoma tissues compared to their matched adjacent non-tumor tissues, and the upregulation of miR-93 was associated with the malignant progression of osteosarcoma. Furthermore, miR-93 was also upregulated in the human osteosarcoma cell lines Saos-2, U2OS, SW1353 and MG63 when compared with that in the human osteoblast cell line hFOB1.19. Transfection with miR-93 inhibitor significantly reduced the miR-93 levels and inhibited the proliferation of U2OS and MG63 osteosarcoma cells. The protein levels of P21 were negatively regulated by miR-93 in U2OS and MG63 cells. Knockdown of miR-93 caused cell cycle arrest at G1 stage in U2OS and MG63 cells, identical to the effect of P21 overexpression. Finally, P21 was found to be significantly downregulated in osteosarcoma tissues compared to their matched adjacent non-tumor tissues, suggesting that the inhibition of P21 may be due to increased miR-93 expression in osteosarcoma tissues. In conclusion, the present study demonstrated that miR-93 enhances the proliferation of osteosarcoma cells, at least in part via inhibiting P21 expression and thus promoting cell cycle progression.

show abstract

Deregulation of miR-93 and miR-143 in human esophageal cancer

Cited by 38 publications

References 63 publications

lncRNA CCAT1 is a biomarker for the proliferation and drug resistance of esophageal cancer via the miR‐143/PLK1/BUBR1 axis

lncRNA CCAT1 is a biomarker for the proliferation and drug resistance of esophageal cancer via the miR‐143/PLK1/BUBR1 axis

Identification of molecular targets for esophageal carcinoma diagnosis using miRNA-seq and RNA-seq data from The Cancer Genome Atlas: a study of 187 cases

MicroRNA-93 promotes cell proliferation by directly targeting P21 in osteosarcoma cells

Contact Info

Product

Resources

About