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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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE279412 | GEO | 2024/11/13

REPOSITORIES: GEO

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			Action	DRS
		Other
	GSE279412_C33AmiR124-C33Asc.tabular.gz	Other
	GSE279412_C33AmiR218-C33Asc.tabular.gz	Other
	GSE279412_C33AmiR23b-C33Asc.tabular.gz	Other
	GSE279412_CaSkimiR124-CaSkisc.tabular.gz	Other

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Project description:PD-L1 Inhibitor Regulates the miR-33a-5p/PTEN Signaling Pathway and Can Be Targeted to Sensitize Glioblastomas to Radiation. Glioblastoma (GBM) is the most common and lethal brain tumor in adults. Ionizing radiation (IR) is a standard treatment for GBM patients and results in DNA damage. However, the clinical efficacy of IR is limited due to therapeutic resistance. The programmed death ligand 1 (PD-L1) blockade has a shown the potential to increase the efficacy of radiotherapy by inhibiting DNA damage and repair responses. The miR-33a-5p is an essential microRNA that promotes GBM growth and self-renewal. In this study, we investigated whether a PD-L1 inhibitor (a small molecule inhibitor) exerted radio-sensitive effects to impart an anti-tumor function in GBM cells by modulating miR-33a-5p. U87 MG cells and U251 cells were pretreated with PD-L1 inhibitor. The PD-L1 inhibitor-induced radio-sensitivity in these cells was assessed by assaying cellular apoptosis, clonogenic survival assays, and migration. TargetScan and luciferase assay showed that miR-33a-5p targeted the phosphatase and tensin homolog (PTEN) 3' untranslated region. The expression level of PTEN was measured by western blotting, and was also silenced using small interfering RNAs. The levels of DNA damage following radiation was measured by the presence of γ-H2AX foci, cell cycle, and the mRNA of the DNA damage-related genes, BRCA1, NBS1, RAD50, and MRE11. Our results demonstrated that the PD-L1 inhibitor significantly decreased the expression of the target gene, miR-33a-5p. In addition, pretreatment of U87 MG and U251 cells with the PD-L1 inhibitor increased radio-sensitivity, as indicated by increased apoptosis, while decreased survival and migration of GBM cells. Mir-33a-5p overexpression or silencing PTEN in U87 MG and U251 cells significantly attenuated PD-L1 radiosensitive effect. Additionally, PD-L1 inhibitor treatment suppressed the expression of the DNA damage response-related genes, BRCA1, NBS1, RAD50, and MRE11. Our results demonstrated a novel role for the PD-L1 inhibitor in inducing radio- sensitivity in GBM cells, where inhibiting miR-33a-5p, leading to PTEN activated, and inducing DNA damage was crucial for antitumor immunotherapies to treat GBM.

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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

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