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Targeted proteomic analysis of 14-3-3sigma in nasopharyngeal carcinoma
Wei-Guo Huang1, Ai-Lan Cheng, Zhu-Chu Chen
1Key Laboratory of Cancer Proteomics of Chinese Ministry of Health, Xiangya Hospital, Central South University, Changsha 410008, China.
Abstract:
14-3-3sigma is a potential tumor suppressor, and loss of 14-3-3sigma expression plays an important role in carcinogenesis and metastasis. To explore the possible mechanism of 14-3-3sigma in nasopharyngeal carcinoma (NPC) invasion and metastasis, targeted proteomic analysis was performed on 14-3-3sigma-associated proteins from NPC cells. As the results, 112 proteins associated with 14-3-3sigma were identified, and four 14-3-3sigma-interacted proteins: keratin 8, epidermal growth factor receptor (EGFR), small GTP-binding protein RAB7, and p53 were confirmed by coimmunoprecipitation and Western blot analysis. The 14-3-3sigma-associated proteins could be grouped into eight clusters based on their molecule functions. Protein-protein interaction (PPI) analysis indicated that 14-3-3sigma/EGFR/keratin 8 interactions may be involved in the invasion and metastasis of NPC. 14-3-3sigma/EGFR/keratin 8 could form complexes in NPC cells. 14-3-3sigma downregulation in NPC may lead to the overexpression of EGFR and keratin 8, which increases the invasion ability of NPC cells possibly by activating the downstream signal molecules and reorganizing cytoskeleton. The data suggest that the biological functions of 14-3-3sigma in NPC are diversified, and 14-3-3sigma could inhibit the in vitro invasive ability of NPC cells possibly through 14-3-3sigma/EGFR/keratin 8 interaction.
Insights
Loss of 14-3-3sigma protein expression in nasopharyngeal carcinoma (NPC) may promote cancer spread. This study identified 14-3-3sigma interactions with EGFR and keratin 8, suggesting a mechanism for NPC invasion.
Area of Science:
- Oncology
- Molecular Biology
- Proteomics
Background:
- 14-3-3sigma acts as a tumor suppressor, and its reduced expression is linked to cancer development and metastasis.
- Understanding the role of 14-3-3sigma in nasopharyngeal carcinoma (NPC) invasion and metastasis is crucial for therapeutic strategies.
Purpose of the Study:
- To investigate the mechanism by which 14-3-3sigma influences NPC invasion and metastasis.
- To identify proteins interacting with 14-3-3sigma in NPC cells.
Main Methods:
- Targeted proteomic analysis was employed to identify 14-3-3sigma-associated proteins in NPC cells.
- Coimmunoprecipitation and Western blot assays were used to confirm interactions with specific proteins, including keratin 8, EGFR, RAB7, and p53.
- Protein-protein interaction (PPI) analysis was performed to understand functional relationships.
Main Results:
- 112 proteins associated with 14-3-3sigma were identified.
- Interactions between 14-3-3sigma, epidermal growth factor receptor (EGFR), and keratin 8 were confirmed.
- These interactions appear to form complexes within NPC cells and may be involved in NPC invasion and metastasis.
Conclusions:
- Downregulation of 14-3-3sigma in NPC may lead to increased EGFR and keratin 8 expression, enhancing cell invasion.
- The 14-3-3sigma/EGFR/keratin 8 interaction is a potential mechanism inhibiting NPC cell invasion.
- 14-3-3sigma exhibits diverse biological functions in NPC, including the inhibition of in vitro invasive capabilities.