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Updated: Nov 5, 2025

Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells
Published on: June 7, 2019
TRIM14 regulates melanoma malignancy via PTEN/PI3K/AKT and STAT3 pathways
Jiangyan Chen1, Lin Huang2, Jin Quan1
1Department of Oncology, Jiangjin Central Hospital of Chongqing, Chongqing, China.
Abstract:
Melanoma is one of the most aggressive cancers with poor overall survival. To date, there are still few effective methods for the treatment of melanoma. TRIM14 was previously reported to be an important oncogene in many tumors. Nevertheless, the roles of TRIM14 in melanoma remain unknown. In this study, we found that TRIM14 was abnormally upregulated in melanoma cell lines. Knockdown of TRIM14 suppressed melanoma cell proliferation, migration, invasion, epithelial-mesenchymal transition, and melanin synthesis. Overexpression of TRIM14 had opposite effects on the cellular functions of melanoma cell lines. Further study revealed that TRIM14 knockdown increased PTEN protein levels, which in turn inactivated AKT and STAT3 pathways. Moreover, blocking AKT or STAT3 pathway with a specific inhibitor could partially reverse the promotion of melanoma malignancy mediated by TRIM14 overexpression. In addition, in vivo assay also supported the above findings. These results indicated that TRIM14 might be a promising target for melanoma treatment.
Insights
This study reveals that TRIM14 (tripartite motif-containing protein 14) is upregulated in melanoma, promoting cancer progression. Inhibiting TRIM14 suppressed melanoma cell growth and invasion, suggesting it as a potential therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Melanoma is an aggressive skin cancer with limited effective treatments.
- The role of TRIM14 (tripartite motif-containing protein 14) in melanoma pathogenesis is currently unknown.
- TRIM14 is recognized as an oncogene in various human cancers.
Purpose of the Study:
- To investigate the functional role of TRIM14 in melanoma.
- To elucidate the underlying molecular mechanisms of TRIM14 in melanoma progression.
- To evaluate TRIM14 as a potential therapeutic target for melanoma.
Main Methods:
- Analysis of TRIM14 expression in melanoma cell lines.
- Knockdown and overexpression of TRIM14 in melanoma cells.
- Assessment of cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT).
- Western blot analysis to detect protein levels and pathway activation (PTEN, AKT, STAT3).
- In vivo xenograft mouse models.
Main Results:
- TRIM14 expression was significantly upregulated in melanoma cell lines.
- TRIM14 knockdown inhibited melanoma cell proliferation, migration, invasion, and EMT.
- TRIM14 overexpression promoted these aggressive cellular phenotypes.
- TRIM14 knockdown led to increased PTEN levels, inactivating AKT and STAT3 pathways.
- Inhibition of AKT or STAT3 partially reversed TRIM14-mediated melanoma malignancy.
- In vivo studies corroborated these findings.
Conclusions:
- TRIM14 acts as an oncogene in melanoma by regulating PTEN/AKT/STAT3 signaling.
- TRIM14 promotes melanoma cell proliferation, migration, invasion, and EMT.
- TRIM14 represents a promising molecular target for novel melanoma therapies.
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