Glypican-3 (GPC3), a membrane-bound heparan sulfate proteoglycan, has long been found to be dysregulated in human lung adenocarcinomas (LUADs). Nevertheless, the function, mutational profile, epigenetic regulation, co-expression profile, and clinicopathological significance of the GPC3 gene in LUAD progression are not well understood. In this study, we analyzed cancer microarray datasets from publicly available databases using bioinformatics tools to elucidate the above parameters. We observed significant downregulation of GPC3 in LUAD tissues compared to their normal counterparts, and this downregulation was associated with shorter overall survival (OS) and relapse-free survival (RFS). Nevertheless, no significant differences in the methylation pattern of GPC3 were observed between LUAD and normal tissues, although lower promoter methylation was observed in male patients. GPC3 expression was also found to correlate significantly with infiltration of B cells, CD8+, CD4+, macrophages, neutrophils, and dendritic cells in LUAD. In addition, a total of 11 missense mutations were identified in LUAD patients, and ~1.4% to 2.2% of LUAD patients had copy number amplifications in GPC3. Seventeen genes, mainly involved in dopamine receptor-mediated signaling pathways, were frequently co-expressed with GPC3. We also found 11 TFs and 7 miRNAs interacting with GPC3 and contributing to disease progression. Finally, we identified 3 potential inhibitors of GPC3 in human LUAD, namely heparitin, gemcitabine and arbutin. In conclusion, GPC3 may play an important role in the development of LUAD and could serve as a promising biomarker in LUAD.
A high-performance interdigitated electrode (IDE) biosensing surface was reported here by utilizing self-assembled silica nanoparticle (SiNP). The modified surface was used to evaluate the complementation of hairpin forming region from Mitoxantrone resistance gene 7 (MXR7; liver cancer-related short gene). The conjugated SiNPs on 3-aminopropyl triethoxysilane functionalization were captured with probe sequence on IDE biosensing surface. The physical and chemically modified surface was used to quantify MXR7 and an increment in the current response upon complementation was noticed. Limit of target DNA detection was calculated (1-10 fM) and this label-free detection is at the comparable level to the fluorescent-based sensing. A linear regression was calculated [y = 0.243x - 0.0773; R² = 0.9336] and the sensitivity was 1 fM on the linear range of 1 fM to 10 pM. With the strong attachment of capture DNA on IDE through SiNP, the surface clearly discriminates the specificity (complementary) versus nonspecificity (complete-, single-, and triple-mismatched sequences). This detection strategy helps to determine liver cancer progression and the similar strategy can be followed for other gene sequence complementation.