GPC5

What is GPC5 protein?

GPC5 gene (glypican 5) is a protein coding gene which situated on the long arm of chromosome 13 at locus 13q31. Cell surface heparan sulfate proteoglycans are composed of a membrane-associated protein core substituted with a variable number of heparan sulfate chains. Members of the glypican-related integral membrane proteoglycan family (GRIPS) contain a core protein anchored to the cytoplasmic membrane via a glycosyl phosphatidylinositol linkage. These proteins may play a role in the control of cell division and growth regulation. The GPC5 protein is consisted of 572 amino acids and GPC5 molecular weight is approximately 63.7 kDa.

What is the function of GPC5 protein?

GPC5 plays a role in a variety of biological processes, including cell signaling, cell proliferation, migration and differentiation. In lung cancer, GPC5 is generally considered a tumor suppressor. GPC5 can inhibit tumor growth by inhibiting the Wnt/β-catenin signaling pathway, which plays an important role in the occurrence and development of lung cancer. GPC5 is able to affect a variety of cell signaling pathways including Wnt, Hedgehog, and Fibroblast Growth Factors (FGF), which play key roles in cell proliferation, differentiation, and survival. GPC5 inhibits the progression and metastasis of lung cancer by regulating the intracellular CTDSP1/AhR/ARNT signaling axis and extracellular exosome secretion. GPC5 expression may be subject to epigenetic regulation, such as DNA methylation, which may play an important role in tumorigenesis.

Fig1. Schematic diagram shows molecular mechanisms of IR caused by palmitate exposure. (Yoshio Hirabayashi, 2022)

GPC5 related signaling pathway

GPC5 inhibits tumor growth by inhibiting the Wnt/β-catenin signaling pathway, which has received particular research attention in lung adenocarcinoma. The Wnt/β-catenin signaling pathway is a key cellular regulatory network involved in cell proliferation, differentiation, and tumorigenesis. GPC5 exerts its tumor suppressor effect by inhibiting β-catenin activity in this pathway, reducing tumor cell proliferation and enhancing apoptosis. In addition to the Wnt/β-catenin signaling pathway, GPC5 is involved in other signal transduction mechanisms. For example, it acts intracellular through the CTDSP1/AhR/ARNT signaling axis and influences the extracellular environment through exosome secretion, inhibiting the progression and metastasis of lung cancer.

GPC5 related diseases

GPC5 is a protein associated with a variety of diseases, including cancer, diabetes, obesity, and Alzheimer's disease. In the field of cancer, especially in the study of lung cancer, the role of GPC5 has received extensive attention. It is commonly expressed as a tumor suppressor gene in lung adenocarcinoma and is able to inhibit tumor growth and metastasis by inhibiting the Wnt/β-catenin signaling pathway. In addition, GPC5 is involved in regulating the intracellular CTDSP1/AhR/ARNT signaling axis and influences tumor progression and metastasis through extracellular exosome secretion. In non-small cell lung cancer, the expression of GPC5 is reduced, while this phenomenon is not seen in other histological subtypes of lung cancer. The function of GPC5 may be subject to epigenetic regulation, such as DNA methylation, which may play an important role in tumorigenesis.

Bioapplications of GPC5

rhGPC5 protein has many potential applications in the biomedical field. It is mainly studied for use in cancer therapy, especially as a tumor suppressor in the treatment of lung cancer. rhGPC5 can inhibit the growth of tumor cells by inhibiting the Wnt/β-catenin signaling pathway, which is particularly important in the treatment of lung adenocarcinoma. In addition, rhGPC5 is involved in regulating the intracellular CTDSP1/AhR/ARNT signaling axis and influences tumor progression and metastasis through exosome secretion. These studies offer the possibility of developing new cancer treatment strategies, including using rhGPC5 as a drug target or in combination with other treatments to improve treatment effectiveness.