TRPM2 promotes the proliferation and invasion of pancreatic ductal adenocarcinoma.
Mol Med Rep
; 17(6): 7537-7544, 2018 Jun.
Article
in En
| MEDLINE
| ID: mdl-29620272
ABSTRACT
The aim of the present study was to investigate transient receptor potential cation channel subfamily M member 2 (TRPM2), a promising therapeutic target and biomarker for pancreatic ductal adenocarcinoma (PDAC) prognosis, in addition to determining its effects regarding tumor progression and invasion. PDAC is a fatal disease with a poor prognosis, and its associated pathogenic molecular mechanisms remain to be determined. In the present study, combined analysis using genomic and transcriptomic data from two PDAC studies was performed to discover a survivalassociated biomarker of PDAC. Survival analysis for genes mutated in ≥10 patients was performed using a KaplanMeier curve and tested for significance using a logrank test. Furthermore, geneexpression correlation analysis was performed to determine the genes with the strongest correlations to TRPM2. In addition, a Cell Counting Kit8 assay, a scratch woundhealing assay and a Transwell assay were performed in the present study to investigate the proliferative, invasive and metastatic ability of PANC1 cells in TRPM2overexpressing and downregulated groups. The mutated TRPM2 gene had a strong negative correlation with patient survival probability compared with the normal control group (P=1.06x104). Expression of TRPM2 was strongly correlated with expression of probable phospholipidtransporting ATPase IM, γparvin, tudor domain containing 9, Tolllike receptor 7 and Scmlike with four MBT domains protein 2 according to the criterion of a correlation coefficient >0.5. Furthermore, the results of the present study demonstrated that the TRPM2 overexpression in a PDAC cell line (PANC1) promoted cell proliferation, invasion and metastatic ability. TRPM2 represents a potential therapeutic target and prognostic marker for patients with PDAC. TRPM2 regulates cell proliferation, invasion and migration; however, the underlying mechanism requires further investigation in future studies.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Pancreatic Neoplasms
/
Carcinoma, Pancreatic Ductal
/
TRPM Cation Channels
Type of study:
Prognostic_studies
Limits:
Female
/
Humans
/
Male
Language:
En
Journal:
Mol Med Rep
Year:
2018
Document type:
Article