Bioinformatics analysis and experimental verification of TIGD1 in non-small cell lung cancer.

Introduction: Non-small cell lung cancer (NSCLC) is a prevalent respiratory system tumor. Triggered transposable element derivative 1 (TIGD1) exhibits significant overexpression in various tumor cells and tissues, suggesting its involvement in cancer progression. Methods: Clinical data and gene expression profiles of lung adenocarcinoma were collected from TCGA, UCSC XENA, and GEO databases. Computational techniques and empirical studies were employed to analyze the role of TIGD1 in NSCLC. Cellular experiments were conducted using the H1299 cell line, including RNA interference, cell viability assays, quantitative PCR, wound-healing assays, western blotting, and plate clone formation assays. Results: Bioinformatics analysis revealed TIGD1's potential as a biomarker for diagnosing and predicting lung cancer. It also indicated promise as a target for immune-related therapy and targeted drug therapy. Cellular studies confirmed TIGD1's involvement in cancer cell proliferation, invasion, and migration. Furthermore, an association between TIGD1 and the PI3K/AKT signaling pathway was suggested. Discussion: The findings suggest that TIGD1 plays a vital role in NSCLC progression, making it a potential diagnostic biomarker and therapeutic target. The association with the PI3K/AKT signaling pathway provides insights into the underlying molecular mechanisms. Integrating computational analysis with empirical studies enhances our understanding of TIGD1's significance in NSCLC and opens avenues for further research into targeted therapies.

Mucin1 relieves acute lung injury by inhibiting inflammation and oxidative stress.

Acute lung injury/acute respiratory distress syndrome (ALI/ARDS) is a kind of diffuse inflammatory injury caused by various factors, characterized by respiratory distress and progressive hypoxemia. It is a common clinical critical illness. The aim of this study was to investigate the effect and mechanism of the Mucin1 (MUC1) gene and its recombinant protein on lipopolysaccharide (LPS)-induced ALI/ARDS. We cultured human alveolar epithelial cell line (BEAS-2B) and used MUC1 overexpression lentivirus to detect the effect of MUC1 gene on BEAS-2B cells. In addition, we used LPS to induce ALI/ARDS in C57/BL6 mice and use hematoxylin and eosin (H&E) staining to verify the effect of their modeling. Recombinant MUC1 protein was injected subcutaneously into mice. We examined the effect of MUC1 on ALI/ARDS in mice by detecting the expression of inflammatory factors and oxidative stress molecules in mouse lung tissue, bronchoalveolar lavage fluid (BALF) and serum. Overexpression of MUC1 effectively ameliorated LPS-induced damage to BEAS-2B cells. Results of H&E staining indicate that LPS successfully induced ALI/ARDS in mice and MUC1 attenuated lung injury. MUC1 also reduced the expression of inflammatory factors (IL-1ß, TNF-α, IL-6 and IL-8) and oxidative stress levels in mice. In addition, LPS results in an increase in the activity of the TLR4/NF-κB signaling pathway in mice, whereas MUC1 decreased the expression of the TLR4/NF-κB signaling pathway. MUC1 inhibited the activity of TLR4/NF-κB signaling pathway and reduced the level of inflammation and oxidative stress in lung tissue of ALI mice.