Silencing RPARP‐AS1 targeted miR‐10b‐5p to induce NSCLC cell proliferation, migration, and invasion, leading to tumor progression and poor prognosis.
Abstract
Objective To investigate the roles of RPARP‐AS1 and miR‐10b‐5p in regulating the prognosis and tumor progression of non‐small cell lung cancer (NSCLC). Methods A total of 138 NSCLC patients were enrolled. Surgical specimens were stored in liquid nitrogen. All patients received 5 years of clinical follow‐up for prognostic assessment. In addition, multivariate Cox regression analysis was conducted to identify independent factors affecting NSCLC prognosis, and gene expression levels were quantified by reverse transcription quantitative polymerase chain reaction (RT‐qPCR). Cell Counting Kit‐8 (CCK‐8) assays were performed to examine cell proliferation, and transwell assays were used to assess cell migration and invasion. Furthermore, nuclear‐cytoplasmic fractionation experiments were conducted to localize RPARP‐AS1 distribution. The interaction between RPARP‐AS1 and miR‐10b‐5p was examined by dual luciferase reporter assays, and downstream targets in NSCLC were predicted using databases. Results RPARP‐AS1 was downregulated, while miR‐10b‐5p was upregulated in both NSCLC patient tissues and cells. Patients with reduced RPARP‐AS1 expression or increased miR‐10b‐5p expression had lower survival rates, accompanied by worsened tumor size, differentiation, and metastasis. oe‐RPARP‐AS1 inhibited tumor cell proliferation, migration, and invasion. However, RPARP‐AS1‐induced functional alterations in NSCLC cells were mediated by miR‐10b‐5p. A total of 47 overlapping genes were identified to potentially mediate downstream signaling pathways of the RPARP‐AS1/miR‐10b‐5p axis in NSCLC cells. Conclusion Silencing RPARP‐AS1 targeted miR‐10b‐5p to induce NSCLC cell proliferation, migration, and invasion, leading to tumor progression and poor prognosis.
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