Abstract
Small‐cell lung cancer (SCLC) is an aggressive malignancy characterized by high cellular proliferation and early distant metastasis. Our study aimed to explore the effect of miR‐22‐3p (miR‐22, for short) on SCLC radiosensitivity and its molecular mechanisms. The expression level of miR‐22 was evaluated in a human normal lung epithelial cell line and a human SCLC cell line, and cell apoptosis and migration were detected. The expression of the miR‐22 direct target WRNIP1 mRNA and protein were explored. Five differentially expressed genes were detected. The miR‐22 expression in NCI‐H446 was significantly decreased, and miR‐22 overexpression significantly promoted cell apoptosis. miR‐22 overexpression could significantly inhibit the cell migration of SCLC cells, and miR‐22 had a negative regulatory effect on WRNIP1 mRNA and protein levels. KLK8 was downregulated, and the messenger RNA (mRNA) of four other genes (PC, SCUBE1, STC1, and GPM6A) was upregulated mRNA in cells overexpressing miR‐22, which was in accordance with the bioinformatics analysis. miR‐22 could enhance the radiosensitivity of SCLC by targeting WRNIP1.
Highlights
Lung cancer (LC) has the highest morbidity and mortality in the world, which seriously threatens human life and health.[1]
We explored the effect of miR‐22 on Small‐cell lung cancer (SCLC) cell apoptosis by APC Annexin V/propidium iodide (PI) double staining
We detected Ki‐67 expression in miR‐22 mimic‐ and inhibitor‐transfected cells and explored the effect of miR‐22 on apoptosis in SCLC by APC Annexin V/PI staining. These results indicated that miR‐22, as a tumor suppressor, could change cell proliferation and promote apoptosis in SCLC cells, and the results of our study were consistent with the previous outcome
Summary
Lung cancer (LC) has the highest morbidity and mortality in the world, which seriously threatens human life and health.[1]. Ionizing radiation (IR) is one of the major modalities of SCLC treatment.[5] It causes DNA damage by producing intermediate ions and oxygen free radicals, leading to tumor cells apoptosis.[6]. Regulating the expression of miRNAs has a significant impact on the clinical radiation response, as it enhances cell susceptibility.[14]. MiR‐22‐3p (miR‐22, for short), which is a 22 nucleotide noncoding RNA located on chromosome 17, has been found to regulate tumor‐related gene expression in different cancer models.[16]. Our findings demonstrate the therapeutic utility of miR‐22 as a potential tumor radiosensitizer in a SCLC model. These results suggest that the miR‐22 cargo combined with radiotherapy may represent a new strategy for SCLC treatment
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