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MicroRNA‑130a‑3p inhibition suppresses cervical cancer cell progression

ABSTRACT: MicroRNA‑130a‑3p inhibition suppresses cervical cancer cell progression

PROVIDER: PRJNA930490 | ENA |

REPOSITORIES: ENA

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MicroRNA‑130a‑3p inhibition suppresses cervical cancer cell progression

Project description:MicroRNAs (miRNAs or miRs) play essential roles in the initiation and progression of human tumors, including cervical cancer. However, the mechanisms underlying their actions in cervical cancer remain unclear. The present study aimed to evaluate the functional role of miR‑130a‑3p in cervical cancer. Cervical cancer cells were transfected with a miRNA inhibitor (anti‑miR‑130a‑3p) and a negative control. Adhesion‑independent cell proliferation, migration and invasion were evaluated. The findings presented herein demonstrated that miR‑130a‑3p was overexpressed in HeLa, SiHa, CaSki, C‑4I and HCB‑514 cervical cancer cells. The inhibition of miR‑130a‑3p significantly reduced the proliferation, migration and invasion of cervical cancer cells. The canonical delta‑like Notch1 ligand (DLL1) was identified as a possible direct target of miR‑103a‑3p. The DLL1 gene was further found to be significantly downregulated in cervical cancer tissues. On the whole, the present study demonstrates that miR‑130a‑3p contributes to the proliferation, migration and invasion of cervical cancer cells. Therefore, miR‑130a‑3p may be used as a biomarker to determine cervical cancer progression.

2023-03-10 | GSE224301 | GEO

MicroRNA‑130a‑3p inhibition suppresses cervical cancer cell progression.

Project description: Not available

| S-EPMC10152451 | biostudies-literature

Gene expression analysis of THP-1 cells (monocytic cell line) transfected with microRNA mimics: let-7d-3p, let-7e-5p,miR-146a-5p,miR-130a-3p, miR-151a-3p.

Project description:In our previous study, hsa-let-7d-3p, hsa-let-7e-5p,hsa-miR-146a-5p,hsa-miR-130a-3p, hsa-miR-151a-3p,were significantly upregulated in the plasma of atopic patients. To study the each function of let-7d-3p, let-7e-5p,miR-146a-5p,miR-130a-3p, miR-151a-3p which are significantly upregulated in the plasma of atopic patients, we performed mimic-transfected THP-1 cells, a mononuclear cell line, and performed comprehensive genetic analysis.

2023-02-06 | GSE217971 | GEO

mRNA expression profile in IL-4-treated macrophages transfected with miR-142-5p ASO or miR-130a-3p mimics

2014-07-12 | GSE59347 | GEO

mRNA expression profile in IL-4-treated macrophages transfected with miR-142-5p ASO or miR-130a-3p mimics

Project description:To identify target genes of miR-142-5p and miR-130a-3p that are involved in M2 polarization, we examined the mRNA expression profile changes after altering miR-142-5p or miR-130a-3p expression in IL-4-treated macrophages. Macrophages were transfected with control ASO, miR-142-5p ASO, control mimics or miR-130-3p mimics using lentiviral vectors. After 24 hr, the cells were treated with IL-4 for 24h.mRNA was purified from total RNA after removal of rRNA (mRNA-ONLY™ Eukaryotic mRNA Isolation Kit, Epicentre). Then, each sample was amplified and transcribed into fluorescent cRNA along the entire length of the transcripts without 3’ bias utilizing a random priming method. The labeled cRNAs were hybridized onto the Human RNA Array v2.0 (8 x 60K, Arraystar). After having washed the slides, the arrays were scanned by the Agilent Scanner G2505B.

2014-07-12 | E-GEOD-59347 | biostudies-arrayexpress

Cross-species identification of DLPFC-specific miR-130a-3p as a causal driver of major depressive disorder implicating microglial neuroimmune suppression

Project description:MicroRNAs (miRNAs) are postulated as pivotal epigenetic regulators in Major Depressive Disorder (MDD), yet distinguishing causal drivers from secondary associations remains a significant challenge due to cross-species barriers and tissue specificity. Here, we present a cross-species integrative framework rooted in human genetics and functionally validated in rodents to identify pathogenic miRNAs. By integrating large-scale cis-eQTLs and MDD GWAS data using Mendelian Randomization, we identified miR-130a-3p as a robust causal risk factor. Multivariable MR and neuroimaging integration further pinpointed the Dorsolateral Prefrontal Cortex (DLPFC) as the primary mediator of its pathogenic effects, characterized by disrupted related functional connectivity. Validating these findings, viral-mediated overexpression of miR-130a-3p in the murine medial prefrontal cortex (the functional homolog of human DLPFC) was sufficient to induce core depressive-like behaviors, including anhedonia and despair. Transcriptomic profiling revealed that miR-130a-3p predominantly downregulated genes enriched in immune-related pathways and specifically in microglia, suggesting a suppression of local neuroimmune signaling and an interruption of microglia-driven homeostasis. Finally, integrating these results with human Transcriptome-Wide Association Studies (TWAS) revealed that the expression levels of some miR-130a-3p downstream genes in the human DLPFC are significantly associated with MDD risk, completing a translational closed-loop that reinforces the relevance of the identified pathway. Collectively, our study identifies miR-130a-3p as a causal neuroimmune modulator in MDD and demonstrates the utility of a genetics-anchored, cross-species pipeline for dissecting the molecular etiology of psychiatric disorders.

2026-01-18 | GSE316217 | GEO

Direct targeting of SLC7A11 by miR-143-3p promotes ferroptosis and suppresses malignancy in cervical squamous cell carcinoma

Project description:We performed RNA sequencing (RNA-seq) on cervical tissues from 3 patients with SCC (IB stage, HPV16-positive) and 3 normal controls (HPV16-negative). Differential gene expression, functional enrichment, and protein-protein interaction (PPI) network analyses were conducted to screen key microRNAs (miRNAs) and target genes. Expression of miR-143-3p and SLC7A11 in SCC and normal control tissues was determined by quantitative real-time polymerase chain reaction (qRT-PCR), immunohistochemical staining, and Western blotting (WB). Furthermore, the effect of miR-143-3p mimics and inhibitors on cell proliferation and ferroptosis was evaluated via Cell Counting Kit (CCK)-8 and scratch assays, along with WB, while concurrently detecting ferroptosis-related biochemical markers. Finally, the role of miR-143-3p in epithelial-mesenchymal transition (EMT) of cervical cancer cells was evaluated by WB and immunofluorescence.

2026-07-31 | E-MTAB-17403 | biostudies-arrayexpress

Target genes of chromosome 3p loss in cervical cancer

Project description:Array CGH data were used to depict the prognostic 3p region and its candidate target genes in cervical cancer

2013-03-08 | E-MTAB-1161 | biostudies-arrayexpress

Direct targeting of SLC7A11 by miR-143-3p promotes ferroptosis and suppresses malignancy in cervical squamous cell carcinoma

Project description:Direct targeting of SLC7A11 by miR-143-3p promotes ferroptosis and suppresses malignancy in cervical squamous cell carcinoma

| PRJEB122641 | ENA

Differentially Expressed Genes in C-33A and CaSki Cells Overexpressing miR-124-3p, miR-23b-3p, or miR-218-5p Modulate Processes and Pathways Involved in Cervical Cancer Progression

Project description:Aberrant expression of oncomicroRNAs and tumor suppressor miRNAs (tsmiRs) contributes to the carcinogenesis and progression of cervical cancer (CC). miR-124-3p, miR-23b-3p, and miR-218-5p are tsmiRs that modulate oncogenes regulating cellular processes implicated in CC progression. This research aimed to explore transcriptomic changes in C-33A and CaSki cells following the overexpression of miR-124-3p, miR-23b-3p, and miR-218-5p, and to identify the biological processes (BPs) and pathways modulated by differentially expressed genes (DEGs). A total of 100 nM of miR-124-3p, miR-23b-3p, and miR-218-5p mimetics were transfected into C-33A and CaSki cells, and transcriptome changes were analyzed using RNA-seq. The Galaxy and R-Studio platforms were employed to identify DEGs, while BPs and pathways regulated by DEGs were identified through the DAVID platform. Transcriptional changes revealed both differences and similarities between cell lines and miRNAs. In C-33A cells, miR-124-3p and miR-218 regulated direct and indirect targets involved in the cell cycle and apoptosis. In CaSki cells, apoptosis and viral carcinogenesis were regulated by genes modulated directly or indirectly by miR-124-3p and miR-23b-3p. These tsmiRs demonstrated synergistic activity, regulating multiple transcripts that modulate processes and pathways involved in CC progression, with or without HPV. These findings suggest that miR-124-3p, miR-23b-3p, and miR-218-5p may represent promising therapeutic alternatives for CC treatment.

2024-11-13 | GSE279412 | GEO

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