5p and 3p Strands of miR-34 Family Members Have Differential Effects in Cell Proliferation, Migration, and Invasion in Cervical Cancer Cells

Córdova-Rivas, Sergio; Fraire-Soto, Ixamail; Torres, Andrea Mercado-Casas; Servín-González, Luis Steven; Granados-López, Angélica Judith; López‐Hernández, Yamilé; Estrada, Claudia Araceli Reyes; Gutiérrez-Hernández, Rosalinda; Castañeda-Delgado, Julio Enrique; Ramirez-Hernandez, Leticia A; Varela-Silva, José Antonio; López, Jesús Adrián

doi:10.3390/ijms20030545

Cited by 50 publications

(47 citation statements)

References 84 publications

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“…The microRNA (miR)-34 family is composed of 5p and 3p strands of miR-34a, miR-34b and miR-34c. 10 MicroRNA-34b potently inhibited migration and invasion in metastatic prostate cancer cells by regulating the TGF-β pathway. 12 MicroRNA-34b acted as a tumour suppressor in the oestrogen-dependent growth of breast cancer cells.…”

Section: Discussionmentioning

confidence: 99%

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MiR‐34b‐3p represses cell proliferation, cell cycle progression and cell apoptosis in non‐small‐cell lung cancer (NSCLC) by targeting CDK4

Feng

et al. 2019

J Cellular Molecular Medi

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Lung cancer is the most common incident cancer, with a high mortality worldwide, and non‐small‐cell lung cancer (NSCLC) accounts for approximately 85% of cases. Numerous studies have shown that the aberrant expression of microRNAs (miRNAs) is associated with the development and progression of cancers. However, the clinical significance and biological roles of most miRNAs in NSCLC remain elusive. In this study, we identified a novel miRNA, miR‐34b‐3p, that suppressed NSCLC cell growth and investigated the underlying mechanism. miR‐34b‐3p was down‐regulated in both NSCLC tumour tissues and lung cancer cell lines (H1299 and A549). The overexpression of miR‐34b‐3p suppressed lung cancer cell (H1299 and A549) growth, including proliferation inhibition, cell cycle arrest and increased apoptosis. Furthermore, luciferase reporter assays confirmed that miR‐34b‐3p could bind to the cyclin‐dependent kinase 4 (CDK4) mRNA 3′‐untranslated region (3′‐UTR) to suppress the expression of CDK4 in NSCLC cells. H1299 and A549 cell proliferation inhibition is mediated by cell cycle arrest and apoptosis with CDK4 interference. Moreover, CDK4 overexpression effectively reversed miR‐34‐3p‐repressed NSCLC cell growth. In conclusion, our findings reveal that miR‐34b‐3p might function as a tumour suppressor in NSCLC by targeting CDK4 and that miR‐34b‐3p may, therefore, serve as a biomarker for the diagnosis and treatment of NSCLC.

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Section: Discussionmentioning

confidence: 99%

“…The microRNA (miR)‐34 family is composed of 5p and 3p strands of miR‐34a, miR‐34b and miR‐34c . Córdova‐Rivas S et al found that the 5p and 3p strands of miR‐34 family members had differential effects on cell proliferation, migration and invasion in cervical cancer cells.…”

Section: Discussionmentioning

confidence: 99%

MiR‐34b‐3p represses cell proliferation, cell cycle progression and cell apoptosis in non‐small‐cell lung cancer (NSCLC) by targeting CDK4

Feng

et al. 2019

J Cellular Molecular Medi

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“…Among them, hsa-mir-34c was strongly associated with the signature as its out-degree is the highest in the network as mentioned in the Figure 2. The miRNA hsa-mir-34c has differential effects in migration and cell proliferation in Cervical Cancer was already proved in the literature [22].…”

Section: Resultsmentioning

confidence: 89%

DeMoS: Dense Module based Gene Signature Detection through Quasi-Clique: An Application to Cervical Cancer Prognosis

Saha¹,

Mallik²,

Bandyopadhyay³

2020

Preprint

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Background: Gene signature is useful to represent the molecular alternation in the disease genomes at specified conditions and is often used to distinguish samples into various groups for better research prospective as well as better clinical treatment. There is lack of efficient techniques that can take into account the complex gene expression profile and able to identify the most relevant signatures. Methods: In this article, we presented a new framework to identify Dense Module based gene Signature (DeMoS) and their targeting miRNAs through Quasi-Clique detection algorithm and their application in prognosis survival study. Here we applied a cervical cancer data repository with prognosis clinical data to conduct our experiment. We first performed Empirical Bayes test using Limma method to identify dysregulated genes (or, miRNAs). MiRNA-mediated dysregulated target genes had been extracted from those dysregulated miRNAs. Thereafter, We detected dense co-expressed modules using Quasi-Clique identification technique. The average correlation coefficient was then computed for each resultant module. The module containing the highest correlation was formulated as the resultant gene signature. Next, We applied three well-known classifiers (SVM, PAM and Random Forest (RF)) using 10-fold cross-validation, and obtained AUC. Finally, we performed survival prognosis study for the resultant gene signature. Results: The resultant signature consisted of ten genes, FGF9, FGF18, PPP1R9A, ERBB4, DCDC2, TOX3, ARMC3, DNALI1, RGL3 and ENPP3. In addition, We identified a total of eight dysregulated miRNAs that targeted the aforementioned gene signature. Hsa-mir-34c was found to be strongly associated with the genes signature since its out-degree centrality score was highest. On the other hand, the p-value of the Cox regression in the prognosis study for the resultant gene signature was found to be significant (=4.2e-02). Finally, DeMoS evaluated the highest AUC values (viz., 0.95 for SVM, 0.955 for RF, 0.955 for PAM) for our resultant gene signature in compared to the other state-of-the-art techniques. Conclusions: Our framework estimated most promising gene signature that could classify multiple groups/subtypes of samples with higher AUC as well as statistically significant p-value in regression based prognosis analysis. Our method is useful to determine signature for any RNA-seq profile. Code is available at https://github.com/sahasuparna/DeMoS.

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“…The two possible mature miRNAs of miR-125a, miR-125a-3p and miR-125a-5p, have inverse effects on invasion and migration of lung cancer cells (41). The 3p arm presents more individually regulated targets based on poorly sequence conservation (42). Therefore, the present study hypothesized that miR-34a-3p may exert a protective effect that may different from that of miR-34a-5p in RA.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑34a‑3p inhibits proliferation of rheumatoid arthritis fibroblast‑like synoviocytes

2019

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Rheumatoid arthritis (RA) is a chronic inflammatory joint disease characterized by synovial inflammation. Fibroblast-like synoviocytes (FLS) serve a vital role in the initiation and perpetuation of the immune response in patients with RA. The present study aimed to investigate the potential role of microRNA (miR)-34a-3p in the pathogenesis of RA. FLS were collected from patients with RA and osteoarthritis (OA). The miR-34a-3p mimics and inhibitor vectors were constructed and transfected into RAFLS using Lipofectamine ® 2000. Cell proliferation was determined by Cell Counting kit-8 assay and cell cycle progression was analyzed by flow cytometry. In addition, the expression levels of cell cycle control genes, matrix metalloproteinase (MMP)-1 and MMP-9, and pro-inflammatory cytokines were detected by reverse transcription-quantitative polymerase chain reaction and western blot analysis. The potential targets of miR-34a-3p were predicted by TargetScan and MiRWalk; the target genes were further verified using a luciferase reporter assay. The expression levels of miR-34a-3p were generally lower in RAFLS compared with in OAFLS. miR-34a-3p overexpression significantly inhibited the proliferation of FLS (P<0.01) by suppressing the expression levels of cyclin-dependent kinase 2, cell division cycle 25A and cyclin D1 (P<0.01), and arresting FLS cell cycle progression at the G 1 phase. Furthermore, the expression levels of MMP-1 and 9 were markedly decreased, as were the mRNA and protein expression levels of pro-inflammatory cytokines (tumor necrosis factor α and interleukin 6; P<0.01). Murine double minute 4 (MDM4) was predicted and verified as a potential target gene of miR-34a-3p; the 547–554 nt position of the MDM4 3′-untranslated region harbored one potential binding site for miR-204-3p. The results of the present study indicated that miR-34a-3p may be considered a promising therapeutic target for RA through inhibiting FLS proliferation and suppressing the production of pro-inflammatory cytokines and MMPs.

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5p and 3p Strands of miR-34 Family Members Have Differential Effects in Cell Proliferation, Migration, and Invasion in Cervical Cancer Cells

Cited by 50 publications

References 84 publications

MiR‐34b‐3p represses cell proliferation, cell cycle progression and cell apoptosis in non‐small‐cell lung cancer (NSCLC) by targeting CDK4

MiR‐34b‐3p represses cell proliferation, cell cycle progression and cell apoptosis in non‐small‐cell lung cancer (NSCLC) by targeting CDK4

DeMoS: Dense Module based Gene Signature Detection through Quasi-Clique: An Application to Cervical Cancer Prognosis

MicroRNA‑34a‑3p inhibits proliferation of rheumatoid arthritis fibroblast‑like synoviocytes

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