Background: Lung adenocarcinoma (LUAD) is the most common type of lung cancer, and its pathogenesis is still unclear. The present study aimed to investigate the role of miR-202-3p and its downstream target gene, ribonucleotide reductase regulatory subunit M2 (RRM2), in the occurrence and development of LUAD and elucidate the correlation between RRM2 and the clinicopathological stage and prognosis of LUAD. Methods:The expression of miR-202-3p was analyzed using the CancerMIRNome database and quantitative polymerase chain reaction (qPCR). The effects of miR-202-3p and RRM2 on the proliferation, migration, and invasion of A549 cells were analyzed. A dual luciferase reporter assay was used to verify the targeting of miR-202-3p and RRM2. Additionally, the correlation between RRM2 expression and clinicopathology was analyzed. Results: (I) MiR-202-3p was lowly expressed in LUAD and the LUAD cell lines. qPCR confirmed that microRNA (miRNA) transfection was effective and sufficient for subsequent experiments. (II) MiR-202-3p inhibited the proliferation, invasion, and migration of LUAD cells. (III) There was a targeting relationship between miR-202-3p and RRM2, and miR-202-3p affected the expression of the RRM2 protein. RRM2 was highly expressed in lung cancer tissue. (IV) RRM2 was associated with the clinicopathological staging of lung cancer. The prognosis of patients with low RRM2 expression was better, and the prognostic sensitivity of RRM2 to lung cancer was high. RRM2 may exert its effects via the Notch pathway. (V) Si-RRM2 inhibited the expression of the RRM2 protein. RRM2 promoted the proliferation, migration, and invasion of LUAD cells. A miR-202-3p inhibitor restored the inhibitory effect of si-RRM2 on LUAD cells. Conclusions: MiR-202-3p was lowly expressed in lung cancer tissue. MiR-202-3p overexpression inhibited the proliferation and metastasis of lung cancer cells. RRM2 was highly expressed in lung cancer tissue and promoted the proliferation and metastasis of lung cancer cells. MiR-202-3p targeted and inhibited RRM2, thereby reducing the proliferation and metastasis of LUAD cells. LUAD patients with low RRM2 expression had a better prognosis, and the expression level of RRM2 was correlated with the clinical characteristics of lung cancer patients.

Background: Globally, lung cancer is one of the foremost reasons of death from malignancy. Despite recent improvements in 5-year OS, it is still not ideal despite the diversification of treatment options. The process of apoptosis refers to the death of cells by programmed death. Under normal circumstances, damaged cells can be removed by apoptosis. However, when cancer occurs, these damaged cells will not be removed due to the deficiency of apoptosis of cancer cells, thus leading to the formation of the cancer. Results: As a result of the present study, 134 lung cancer-related genes were found to be differentially expressed between lung adenocarcinomas and normal lungs. There are two subtypes of LUAD on the basis of the DEGs. As a next step in the forecasting value evaluation of such apoptosis-related regulatory factors, in the process of developing an 8-gene risk signature, we conducted a Cox univariate analysis and a LASSO Cox regression analysis. The low- and high-risk sufferers were created for all patients with LUAD in TCGA cohort. Contrary to the high-risk sufferers, the low-risk LUAD sufferers held a remarkably ameliorated OS (P = 0.008). GSE72094 was used as verification and similar results were obtained. The risk score was determined to be a standalone predictor of OS among LUAD sufferers when combined with clinical features. Immuno-related genes were bounteous in high-risk patients, but their immune status was diminished based on the GO and KEGG analysis. Briefly, apoptosis-related genes are critical to cancer immunity and could be possible to foresee LUAD's medical prognosis. Conclusions: Apoptosis-related genes play an important role in lung adenocarcinoma. This experiment provides a new gene marker for predicting the prognosis of LUAD patients.