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Long non‑coding RNA OIP5‑AS1 facilitates the progression of ovarian cancer via the miR‑128‑3p/CCNG1 axis.

ABSTRACT: Long non‑coding RNA (LncRNA) o‑phthalaldehyde-interacting protein 5 antisense transcript 1 (OIP5‑AS1) serves major roles in the progression of various types of cancer. The present study investigated its biological function in ovarian cancer (OC) and its mechanisms. The levels of OIP5‑AS1, microRNA‑128‑3p (miR‑128‑3p) and cyclin G1 (CCNG1) were examined by reverse transcription‑quantitative PCR. Cell viability, apoptosis, migration and invasion were detected to analyze cellular progression. Glycolytic metabolism was assessed by detecting the levels of glucose consumption and lactate production. CCNG1 and hexokinase 2 protein levels were measured by western blotting. Dual‑luciferase reporter assay, RNA immunoprecipitation and RNA pull‑down assays were performed to affirm the interaction between two molecules. OIP5‑AS1 was found to be upregulated in OC tissues and cells. Knockdown of OIP5‑AS1 suppressed cell viability, migration, invasion and glycolysis while promoting apoptosis in OC cells. OIP5‑AS1 interacted with miR‑128‑3p and functioned as an oncogene by sequestering miR‑128‑3p. In addition, CCNG1 was a target gene for miR‑128‑3p and miR‑128‑3p regulated the CCNG1‑induced effects on OC cells by downregulating CCNG1. OIP5‑AS1 upregulated the expression of CCNG1 via targeting miR‑128‑3p. OIP5‑AS1 knockdown also inhibited tumor growth of OC in vivo by modulating the expression of miR‑128‑3p and CCNG1. Collectively, these data illustrated that the oncogenic role of OIP5‑AS1 in OC was associated with the miR‑128‑3p/CCNG1 axis at least in part. OIP5‑AS1 might be a probable diagnostic and therapeutic biomarker for the treatment of OC patients.

SUBMITTER: Liu Y

PROVIDER: S-EPMC8008222 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Oral squamous cell carcinoma (OSCC) accounts for 90% of oral cavity cancer types, but the overall prognosis for patients with OSCC remains unfavorable. Cisplatin (DDP) is an effective drug in OSCC treatment, but DDP resistance weakens its therapeutic effect. Opa-interacting protein 5 antisense RNA 1 (OIP5-AS1) can trigger DDP resistance. The purpose of the current study was to explore the role and mechanism ofOIP5-AS1 in OSCC DDP resistance. In the present study, the expression levels of OIP5-AS1, microRNA (miR)-27b-3p and tripartite motif-containing 14 (TRIM14) were detected by reverse transcription-quantitative PCR. DDP resistance was measured using an MTT assay. Moreover, cell proliferation, migration and invasion were assessed by MTT, Transwell, and Matrigel assays. Protein expression levels of TRIM14, E-cadherin, N-cadherin and Vimentin were detected by western blot analysis. Putative binding sites between miR-27b-3p andOIP5-AS1 or TRIM14werepredicted with starBase and verified using a dual-luciferase reporter assay. The role of OIP5-AS1 in DDP resistance of OSCC in vivo was measured using a xenograft tumor model. It was observed that OIP5-AS1 was upregulated in DDP-resistant OSCC cells, and the knockdown of OIP5-AS1 improved DDP sensitivity in DDP-resistant OSCC cells. The present study identified that miR-27b-3p was a target of OIP5-AS1. Furthermore, miR-27b-3p silencing reversed the effect of OIP5-AS1 knockdown on DDP sensitivity in DDP-resistant OSCC cells. TRIM14was shown to be a direct target of miR-27b-3p, and TRIM14 overexpression abolished the effect of miR-27b-3p on DDP sensitivity in DDP-resistant OSCC cells. The results suggested that OIP5-AS1 increased TRIM14 expression by sponging miR-27b-3p. In addition, OIP5-AS1 knockdown enhanced DDP sensitivity of OSCC in vivo. Data from the present study indicated that OIP5-AS1 may improve DDP resistance through theupregulationTRIM14 mediated bymiR-27b-3p, providing a possible therapeutic strategy for OSCC treatment.

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Long non‑coding RNA OIP5‑AS1 facilitates the progression of ovarian cancer via the miR‑128‑3p/CCNG1 axis.

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