GABPB1 plays a cancer-promoting role in non-small cell lung cancer.

BACKGROUND: GABPB1, the gene that encodes two isoforms of the beta subunit of GABP, has been identified as an oncogene in multiple malignant tumors. However, the role and mode of action of GABPB1 in malignant tumors, especially in lung cancer, are not well understood and need further research. METHODS: Our research focused on examining the biological function of GABPB1 in NSCLC (Non-Small Cell Lung Cancer). We analysed tumor data from public databases to assess the expression of GABPB1 in NSCLC  and its correlation with patient prognosis and investigated GABPB1 expression and methylation patterns in relation to the tumor microenvironment. In parallel, experiments were conducted using short hairpin RNA (shRNA) to suppress the GABPB1 gene in human lung cancer cells to evaluate the effects on cell proliferation, viability, and apoptosis. RESULTS: GABPB1 was widely expressed in various tissues of the human body. Compared to that in normal tissues, the expression of this gene was different in multiple tumor tissues. GABPB1 was highly expressed in lung cancer tissues and cell lines. Its expression was associated with molecular subtype and cellular signalling pathways, and a high level of GABPB1 expression was related to a poor prognosis in lung adenocarcinoma patients. The expression and methylation of GABPB1 affect the tumor microenvironment. After suppressing the expression of GABPB1 in both A549 and H1299 cells, we found a decrease in cell growth and expression, the formation of clones and an increase in the apoptosis rate. CONCLUSIONS: Our research verified that GABPB1 promotes the tumorigenesis of NSCLC and has an inhibitory effect on tumor immunity. The specific role of GABPB1 may vary among different pathological types of NSCLC. This molecule can serve as a prognostic indicator for lung adenocarcinoma, and its methylation may represent a potential breakthrough in treatment by altering the tumor immune microenvironment in lung squamous cell carcinoma. The role and mechanism of action of GABPB1 in NSCLC should be further explored.

Interleukin-1ß weakens paclitaxel sensitivity through regulating autophagy in the non-small cell lung cancer cell line A549.

Non-small cell lung cancer (NSCLC) poses a threat to human health and paclitaxel chemotherapy has been approved for the treatment of this type of cancer. However, resistance to treatment severely compromises the survival rate and prognosis of patients with NSCLC. The aim of the present study was to investigate the role of IL-1ß in paclitaxel sensitivity of NSCLC cells and elucidate the underlying mechanism. The expression of IL-1ß was found to be upregulated in NSCLC tissues and cells compared with healthy adjacent tissues and a normal epithelial cell line, respectively, as detected by reverse transcription-quantitative PCR and western blot analyses. Subsequently, Cell Counting Kit-8 assay and flow cytometry revealed that IL-1ß weakened the sensitivity of A549 cells to paclitaxel. It was subsequently demonstrated that IL-1ß induced A549 cell autophagy, while tunicamycin-induced autophagy increased the IL-1ß expression level and weakened paclitaxel sensitivity. Thus, the results revealed that IL-1ß reduced the sensitivity to paclitaxel in A549 cells by promoting autophagy and suggested that IL-1ß may be of value for improving the therapeutic efficacy of paclitaxel chemotherapy in NSCLC.

Coiled-coil domain-containing 68 promotes non-small cell lung cancer cell proliferation in vitro.

Coiled-coil domain-containing 68 (CCDC68) is a novel secretory protein that acts as a tumor suppressor gene in several types of malignant tumors. However, the role of CCDC68 in the development of lung cancer has not been extensively studied. In the present study, to explore the biological functions of CCDC68 in NSCLC, we performed cell proliferation, viability and apoptosis assays on human lung cancer cell lines upon CCDC68 gene silencing with short hairpin RNA. The results demonstrated that following knockdown of CCDC68 expression, cell proliferation was decreased and the apoptotic rates were increased in A549 and H1299 cells. The role and mechanism of CCDC68 in malignant tumors, particularly in lung cancer, should be further explored, and CCDC68 may serve as a novel target for treatment of lung cancer.