GPC2 as a diagnostic and prognostic marker regulated progression of colorectal cancer.
CEP164
Colorectal cancer
GPC2
Marker
Journal
Arab journal of gastroenterology : the official publication of the Pan-Arab Association of Gastroenterology
ISSN: 2090-2387
Titre abrégé: Arab J Gastroenterol
Pays: Egypt
ID NLM: 101298363
Informations de publication
Date de publication:
13 Jan 2024
13 Jan 2024
Historique:
received:
21
05
2023
revised:
12
09
2023
accepted:
27
11
2023
medline:
15
1
2024
pubmed:
15
1
2024
entrez:
14
1
2024
Statut:
aheadofprint
Résumé
Glypican 2 (GPC2) is a member of the glypican gene family and is expressed in multiple kinds of cancer. However, the function and mechanism of GPC2 in colorectal cancer remains unclear. In this study, we aimed to identify the role of GPC2 on tumor cell proliferation and survival in colorectal cancer. Ten pairs of colon cancer and matched normal colon tissues were collected in this research. GEPIA was used to analysis the GPC2 gene expression profile in TGCA data base. RT-qPCR and western blot assay were performed to determine the mRNA and protein expressions. CCK-8, Flow cytometry and colon formation assay were applied to evaluate cell viability. IHC staining was performed to evaluate the protein expression in tissues. The function of GPC2 in vivo was verified by an animal model of colon cancer. Through the bioinformatics analysis and qRT-PCR validation, we found that GPC2 was upregulated in the colon cancer tissues and cells. GPC2 knockdown suppressed cell proliferation in vitro and in vivo was confirmed by the results of CCK-8, colony formation assays, and tumor xenograft models. Moreover, by the analysis of flow cytometry assay and gain-or-loss function experiments, we discovered that CEP164 was highly associated with the expression state of GPC2, and mediated G2/M-phase arrest in GPC2-downregulated tumor cells. GPC2 might be a novel oncogenic gene in colorectal cancer, suggesting that it could be a considerable marker for the diagnosis and prognosis of colorectal cancer.
Sections du résumé
BACKGROUND AND STUDY AIMS
OBJECTIVE
Glypican 2 (GPC2) is a member of the glypican gene family and is expressed in multiple kinds of cancer. However, the function and mechanism of GPC2 in colorectal cancer remains unclear. In this study, we aimed to identify the role of GPC2 on tumor cell proliferation and survival in colorectal cancer.
PATIENTS AND METHODS
METHODS
Ten pairs of colon cancer and matched normal colon tissues were collected in this research. GEPIA was used to analysis the GPC2 gene expression profile in TGCA data base. RT-qPCR and western blot assay were performed to determine the mRNA and protein expressions. CCK-8, Flow cytometry and colon formation assay were applied to evaluate cell viability. IHC staining was performed to evaluate the protein expression in tissues. The function of GPC2 in vivo was verified by an animal model of colon cancer.
RESULTS
RESULTS
Through the bioinformatics analysis and qRT-PCR validation, we found that GPC2 was upregulated in the colon cancer tissues and cells. GPC2 knockdown suppressed cell proliferation in vitro and in vivo was confirmed by the results of CCK-8, colony formation assays, and tumor xenograft models. Moreover, by the analysis of flow cytometry assay and gain-or-loss function experiments, we discovered that CEP164 was highly associated with the expression state of GPC2, and mediated G2/M-phase arrest in GPC2-downregulated tumor cells.
CONCLUSION
CONCLUSIONS
GPC2 might be a novel oncogenic gene in colorectal cancer, suggesting that it could be a considerable marker for the diagnosis and prognosis of colorectal cancer.
Identifiants
pubmed: 38220478
pii: S1687-1979(23)00105-3
doi: 10.1016/j.ajg.2023.11.006
pii:
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
Copyright © 2023 Pan-Arab Association of Gastroenterology. Published by Elsevier B.V. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.