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SIRT6 inhibits metastasis by suppressing SNAIL expression in nasopharyngeal carcinoma cells
Feng Chen1,2,3, Xiaofeng Ma2,3, Yongze Liu2,3
1Department of Otorhinolaryngology-Head and Neck Surgery, Nanjing Drum Tower Hospital, Clinical College of Nanjing Medical University China.
Abstract:
Nasopharyngeal carcinoma (NPC) is a head and neck cancer with severe local invasion and early distant metastasis. SIRT6 serves as a critical modulator of the development and metastasis of multiple types of cancer; however, the roles and underlying mechanisms of SIRT6 in regulating NPC metastasis remain largely unknown. Here, the expression of SIRT6 in high metastatic 5-8F cells and low metastatic 6-10B cells was analyzed. SIRT6 expression was found to be negatively associated with the metastatic capability of NPC cells. Moreover, we identified that SIRT6 inhibited NPC cell metastasis through suppression of SNAIL expression. Mechanistically, we demonstrated that SIRT6 interacted with transcription factor p65 (NF-kB subunit) and deacetylated histone H3 lysine 9 (H3K9) and lysine 56 (H3K56) at the promoter of SNAIL, leading to reduced transcription of SNAIL. In summary, SIRT6 functions as a metastasis suppressor in NPC cells through epigenetic regulation of SNAIL gene expression.
Insights
SIRT6 suppresses nasopharyngeal carcinoma (NPC) metastasis by epigenetically silencing SNAIL. This finding reveals SIRT6 as a potential therapeutic target for reducing NPC spread and improving patient outcomes.
Area of Science:
- Oncology
- Molecular Biology
- Epigenetics
Background:
- Nasopharyngeal carcinoma (NPC) is an aggressive head and neck cancer known for local invasion and early metastasis.
- SIRT6 is implicated in various cancers, but its role in NPC metastasis is unclear.
Purpose of the Study:
- To investigate the role and mechanism of SIRT6 in regulating nasopharyngeal carcinoma cell metastasis.
- To determine the association between SIRT6 expression and NPC metastatic potential.
Main Methods:
- Comparative analysis of SIRT6 expression in high and low metastatic NPC cell lines (5-8F and 6-10B).
- Investigation of SIRT6's interaction with transcription factor p65 (NF-kB subunit).
- Assessment of SIRT6-mediated epigenetic modification (deacetylation) at the SNAIL promoter (H3K9 and H3K56).
Main Results:
- SIRT6 expression is inversely correlated with NPC cell metastatic capability.
- SIRT6 inhibits NPC cell metastasis by suppressing SNAIL expression.
- SIRT6 deacetylates H3K9 and H3K56 at the SNAIL promoter, reducing its transcription.
Conclusions:
- SIRT6 acts as a metastasis suppressor in nasopharyngeal carcinoma.
- Epigenetic regulation of SNAIL by SIRT6 is a key mechanism inhibiting NPC metastasis.
- Targeting SIRT6 may offer a novel therapeutic strategy for NPC treatment.
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