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TRPV3 inhibits colorectal cancer cell proliferation and migration by regulating the MAPK signaling pathway
Wei Yu1, Jieping Huang2, Hui Yu1
1Department of Clinical Pharmacy, Clinical Oncology School of Fujian Medical University, Fujian Cancer Hospital, Fuzhou, China.
Background:
The aim of this study was to investigate the inhibiting effect of transient receptor potential vanilloid 3 (TRPV3) on the proliferation and migration of colorectal cancer (CRC) cells and to explore the underlying mechanism.
Methods:
A microarray dataset from the publicly available Gene Expression Omnibus (GEO) database was used to investigate the prognostic value of TRPV3 in CRC. In addition, 100 CRC tissue samples were collected at our center to further validate its prognostic value at the protein level. Cell proliferation ability was detected by Cell Counting Kit-8 (CCK-8) assay, and cell migration ability was detected by transwell assay. Gene set variation analysis (GSVA) was performed to identify the potential pathways regulated by TRPV3.
Results:
Based on the largest microarray dataset (GSE39582), low expression of TRPV3 was found to be significantly associated with poor prognosis in CRC patients, and this result was successfully validated at our cancer center. Functional experiments showed that knockdown of TRPV3 enhanced cell proliferation and migration, while enforced TRPV3 expression exhibited the opposite effect. GSEA based on public microarray data revealed that the mitogen-activated protein kinase (MAPK) signaling pathway was notably activated in patients with low expression of TRPV3. Further experiments in vivo confirmed that TRPV3 silencing promoted cell proliferation and migration by activating the MAPK signaling pathway.
Conclusions:
Low expression of TRPV3, which stimulates cell proliferation and migration by provoking the MAPK signaling pathway, indicated poor prognosis in CRC patients.
Insights
Low expression of transient receptor potential vanilloid 3 (TRPV3) in colorectal cancer (CRC) is linked to poor prognosis. TRPV3 inhibits cancer cell proliferation and migration by suppressing the MAPK signaling pathway.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Transient receptor potential vanilloid 3 (TRPV3) is a potential target in cancer therapy.
- Colorectal cancer (CRC) is a significant global health concern with a need for improved prognostic markers.
- Understanding the role of TRPV3 in CRC progression is crucial for developing novel treatment strategies.
Purpose of the Study:
- To investigate the inhibitory effect of TRPV3 on colorectal cancer (CRC) cell proliferation and migration.
- To explore the underlying molecular mechanisms, including signaling pathways involved.
- To evaluate the prognostic value of TRPV3 expression in CRC patients.
Main Methods:
- Analysis of a large microarray dataset (GSE39582) and validation using 100 CRC tissue samples.
- In vitro functional assays: Cell Counting Kit-8 (CCK-8) for proliferation and Transwell assay for migration.
- Gene Set Enrichment Analysis (GSEA) to identify regulated pathways, including the mitogen-activated protein kinase (MAPK) pathway.
- In vivo experiments to confirm the role of TRPV3 and MAPK signaling.
Main Results:
- Low TRPV3 expression is significantly associated with poor prognosis in CRC patients, validated at both gene and protein levels.
- TRPV3 knockdown enhanced CRC cell proliferation and migration, while TRPV3 overexpression inhibited these processes.
- TRPV3 silencing promoted CRC cell proliferation and migration by activating the MAPK signaling pathway.
Conclusions:
- Low TRPV3 expression indicates a poor prognosis in colorectal cancer patients.
- TRPV3 acts as an inhibitor of CRC cell proliferation and migration.
- The mechanism involves the suppression of the MAPK signaling pathway by TRPV3.
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