MicroRNA-101 Inhibits Cell Proliferation, Invasion, and Promotes Apoptosis by Regulating Cyclooxygenase-2 in Hela Cervical Carcinoma Cells

Huang, Fei; Chen, Lin; Shi, Yonghua; Kuerban, Gulinar

doi:10.7314/apjcp.2013.14.10.5915

Cited by 43 publications

(25 citation statements)

References 35 publications

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“…Ting Guan' lab obtained a total of 18 key miRNAs which may play important regulatory roles in ovarian cancer (Wan et al, 2012). MicroRNA-101 Inhibits Cell Proliferation, Invasion, and Promotes Apoptosis by Regulating Cyclooxygenase-2 in Hela Cervical Carcinoma Cells (Huang et al, 2013). MiR-186 was downregulated in tumor cells (Cai et al, 2013;Li et al, 2013a), and correlated with poor survival of patients bearing with lung adenocarcinoma (Cai et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

miR-186 Regulates Glycolysis through Glut1 During the Formation of Cancer-associated Fibroblasts

Sun¹,

Hu²,

Xiong³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Emerging evidence has suggested that glycolysis is enhanced in cancer-associated fibroblasts (CAF), and miR-186 is downregulated during the CAF formation. However, it is not clear whether miR-186 is involved in the regulation of glycolysis and what the role of miR-186 plays during the CAF formation. In this study, quantitative PCR analysises show miR-186 is downregulated during the CAF formation. Moreover, miR-186 targets the 3' UTR of Glut1, and its overexpression results in the degradation of Glut1 mRNA, which eventually reduces the level of Glut1 protein. On the other hand, knockdown of miR-186 increased the expression of Glut1. Both time course and dose response experiments also demonstrated that the protein and mRNA levels of Glut1 increase during CAF formation, according to Western blot and quantitative PCR analyses, respectively. Most importantly, besides the regulation on cell cycle progression, miR-186 regulates glucose uptake and lactate production which is mediated by Glut1. These observations suggest that miR-186 plays important roles in glycolysis regulation as well as cell cycle checkpoint activation.

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Section: Discussionmentioning

confidence: 99%

miR-186 Regulates Glycolysis through Glut1 During the Formation of Cancer-associated Fibroblasts

Sun¹,

Hu²,

Xiong³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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“…COX exists as two isoforms, including the constitutive COX-1 and the mitogen-inducible COX-2. In gastric cancer, COX-2 is continuously expressed and was reported to be closely associated with tumor invasiveness and metastasis (7,8). Previous studies have demonstrated that the inhibition of COX-2 by selective COX-2 inhibitors or small interfering RNA (siRNA) may attenuate proliferation and induce apoptosis in human gastric cancer cells (9,10).…”

Section: Introductionmentioning

confidence: 99%

Paclitaxel combined with harmine inhibits the migration and invasion of gastric cancer cells through downregulation of cyclooxygenase-2 expression

2015

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Abstract. Cyclooxygenase-2 (COX-2) has a critical role in the invasiveness and metastasis of gastric cancer. In addition, paclitaxel (PTX) and harmine (HM) were reported to be potential therapeutic drug candidates for cancer therapy; however, the synergistic antitumor effect of PTX and HM combined treatment on the human gastric cancer cells remains to be elucidated. The aim of the present study was to evaluate the effects of PTX and/or HM on the cell migration and invasion in two human gastric cancer cell lines, SGC-7901 and MKN-45. MTT assay was used to detect the growth inhibition induced by PTX and HM . The Transwell assay was employed to assess the effects of PTX and HM on the cell migration and invasion. The expression levels of COX-2 and matrix metalloproteinase-9 (MMP-9) were analyzed by western blot analysis. The results demonstrated that PTX and HM inhibited cell proliferation in a dose-dependent manner. Individually PTX and HM were able to inhibit the migration and invasion of two human gastric cancer cells; however, the combination of PTX and HM exerted synergistic effects on migration and invasion inhibition, with downregulation of COX-2 and matrix metalloproteinase (MMP)-9. In conclusion, the results of the present study indicated that combination chemotherapy using PTX with HM exerted an antitumor effect, which may be implicated for the treatment of gastric cancer. Of note, the combination of the two drugs inhibited migration and invasion more effectively compared with each drug alone, the mechanism of which proceeded via the downregulation of COX-2 expression.

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“…miRNAs are short approximately 19-24 nucleotide non-coding RNA molecules that post-transcriptionally regulate gene expression via mRNA binding (RNA interference). In cancers, miRNAs have been shown to affect several key oncogenic processes including apoptosis, migration and proliferation (Fonseca-Sanchez et al 2013, Huang et al 2013, Pinho et al 2013. Interestingly, widespread dysregulation of miRNAs has been observed in prostate cancer (Schaefer et al 2010, Fendler et al 2011, Wach et al 2012, and these molecules have potential as both biomarkers and therapeutic targets/treatments (Lichner et al 2013, Maugeri-Sacca et al 2013.…”

Section: Introductionmentioning

confidence: 99%

A genetic variant of MDM4 influences regulation by multiple microRNAs in prostate cancer

Stegeman¹,

Moya²,

Selth³

et al. 2015

Endocrine-Related Cancer

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The oncogene MDM4, also known as MDMX or HDMX, contributes to cancer susceptibility and progression through its capacity to negatively regulate a range of genes with tumoursuppressive functions. As part of a recent genome-wide association study it was determined that the A-allele of the rs4245739 SNP (AOC), located in the 3 0 -UTR of MDM4, is associated with an increased risk of prostate cancer. Computational predictions revealed that the rs4245739 SNP is located within a predicted binding site for three microRNAs (miRNAs): miR-191-5p, miR-887 and miR-3669. Herein, we show using reporter gene assays and endogenous MDM4 expression analyses that miR-191-5p and miR-887 have a specific affinity for the rs4245739 SNP C-allele in prostate cancer. These miRNAs do not affect MDM4 mRNA levels, rather they inhibit its translation in C-allele-containing PC3 cells but not in LNCaP cells homozygous for the A-allele. By analysing gene expression datasets from patient cohorts, we found that MDM4 is associated with metastasis and prostate cancer progression and that targeting this gene with miR-191-5p or miR-887 decreases in PC3 cell viability. This study is the first, to our knowledge, to demonstrate regulation of the MDM4 rs4245739 SNP C-allele by two miRNAs in prostate cancer, and thereby to identify a mechanism by which the MDM4 rs4245739 SNP A-allele may be associated with an increased risk for prostate cancer.Key Words " MDM4" microRNA " single nucleotide polymorphism " prostate cancer

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MicroRNA-101 Inhibits Cell Proliferation, Invasion, and Promotes Apoptosis by Regulating Cyclooxygenase-2 in Hela Cervical Carcinoma Cells

Cited by 43 publications

References 35 publications

miR-186 Regulates Glycolysis through Glut1 During the Formation of Cancer-associated Fibroblasts

miR-186 Regulates Glycolysis through Glut1 During the Formation of Cancer-associated Fibroblasts

Paclitaxel combined with harmine inhibits the migration and invasion of gastric cancer cells through downregulation of cyclooxygenase-2 expression

A genetic variant of MDM4 influences regulation by multiple microRNAs in prostate cancer

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