A Multi- Omics Analysis of GPC3 Down-Expression linking Poor Clinical Outcomes in Human Lung Adenocarcinoma
Down-Expression of GPC3 Tumor Suppressor Gene and Its Prognostic Clinical Outcomes in Human Lung Adenocarcinoma via Bioinformatics Approaches / Multi-Omics Analysis
Downregulation of GPC3 Is A Predictor of Poor Prognosis in Human Lung Adenocarcinoma
Sharmin Aktar1α, Niaz Morshed2α, Rumana Mahtarin3α, Raihan Rahman Imon4, Anindo Rahman4
1Department of Microbiology, University of Dhaka, Bangladesh
2Department of Pharmacy, University of Dhaka, Bangladesh
3Department of Biochemistry and Molecular Biology, Shahjalal University of Science and Technology, Sylhet-3114, Bangladesh
4Department of Genetic Engineering and Biotechnology, Jashore University of Science & Technology, Jashore, Bangladesh;
E-Mail: email@example.com (S.A.), firstname.lastname@example.org (N.M.), email@example.com (R.M.)
αThese authors contributed equally to this study.
Abstract: Lung adenocarcinoma
is a major cause of death worldwide. Some evidence for loss of GPC3 expression has been reported in
lung cancer. GPC3, a membrane-bound
proteoglycan whose expression has been associated with malignancies due to both
mutations and atypical protein expression. In this study, applying multi-omics
approaches, we systematically explored the expression of GPC3 and its clinical outcome in lung adenocarcinoma (LUAD) via
widely accessible cancer gene expression and patient survival data through various
bioinformatics databases. To observe the variations of GPC3 expression between various cancers and their normal tissues,
we employed the Oncomine, GEPIA2, UALCAN databases. The incidence of mutations
and copy number alterations of GPC3
were explored with cBioPortal. The co-expression profile of GPC3 in LUAD was exposed via Oncomine.
The most co-expressed gene along with GPC3
downregulation was FHL1, tumor
suppressor. It emphasized that GPC3 was identified as a tumor
suppressor in our study, eventually, GPC3
mRNA and protein levels in LUAD were significantly reduced than those in normal
lung tissue. Prognoscan analysis curve revealed the downregulation of GPC3 expression, which was significantly
correlated with poor survival in patient.
The pathway and gene ontology investigation were done using co-expressed
genes along with GPC3 via the PANTHER
web tool to search the anticipated signaling pathways in LUAD. Overall, our
data recommend that GPC3 might be a
prognostic novel biomarker for therapeutics improvement in LUAD.