Multi-omics analysis of MRPL-13 as a tumor-promoting marker from pan-cancer to lung adenocarcinoma.

BACKGROUND: As a member of the mitochondrial ribosomal protein family, mitochondrial ribosomal protein L13 (MRPL13) is responsible for synthesizing mitochondrial proteins in cells. Several studies have indicated that MRPL13 is associated with the proliferation cycle, migration ability, apoptosis and autophagy of cancer cells. However, a thorough examination of MRPL13 across cancers remains uncertain. Therefore, we tried to clarify the relationship between MRPL13 and pan-cancer, and verified it in lung adenocarcinoma by various methods. Finally, our research is expected to reveal new targets for pan-cancer treatment and improve the prognosis of cancer patients. METHODS: Using bioinformatics tools, we quantified the differential expression of MRPL13 between cancer tissues and corresponding or noncorresponding normal tissues across cancers. We also analyzed the relationships between MRPL13 expression levels and several factors, including diagnosis, prognosis, mutation, functional signaling pathways, immune infiltration, RNA modification, and the relationship with cuproptosis-related genes. Furthermore, we studied the relationship between the expression level of MRPL13 across cancers and the change in cancer functional status through single-cell data. In addition, quantitative experiments (PCR and Western blot) proved that the expression of MRPL13 was significantly different between LUAD and control samples. Finally, the effect of knocking out MRPL13 on cancer cells was compared by gene silencing experiments. In summary, we used a combination of bioinformatics and experimental applications to study the potential roles of MRPL13 in cancer. RESULTS: After conducting a multidimensional analysis, we found that the application of MRPL13 multigroup analysis can effectively improve the diagnostic efficiency of various cancers and predict the prognosis of cancer. Moreover, MRPL13 in pan-cancer is related to the cancer immune infiltration pattern, methylation level and cuproptosis-related genes. Furthermore, single-cell data analysis showed that the modules of metastasis, EMT, cell cycle, DNA repair, invasion, DNA damage and proliferation were positively correlated with the expression of MRPL13 in LUAD (Lung adenocarcinoma), while the modules of hypoxia and inflammation were negatively correlated. Moreover, through quantitative experiments, we observed higher expression of MRPL13 in cancer tissues at the RNA or protein level. Knockdown of MRPL13 in LUAD led to decreased cancer cell survival, delayed tumor division and migration, reduced invasion, and increased cancer cell apoptosis. CONCLUSIONS: Our study demonstrates the potential of using MRPL13 as a molecular biomarker for diagnosing and suggesting the prognosis of certain malignant tumors. Furthermore, our research shows that MRPL13 may be an effective therapeutic target for lung adenocarcinoma.