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Tid1 functions as a tumour suppressor in head and neck squamous cell carcinoma
Chi-Yuan Chen1, Shih-Hwa Chiou, Chih-Yang Huang
1Institute of Oral Biology, National Yang-Ming University, Taipei, Taiwan, ROC.
Abstract:
Human tumourous imaginal disc (Tid1), a human homologue of the Drosophila tumour suppressor protein Tid56, is involved in multiple intracellular signalling pathways such as apoptosis, cell proliferation, and cell survival. Here, we investigated the anti-tumourigenic activity of Tid1 in head and neck squamous cell carcinoma (HNSCC) in vitro and in vivo. Firstly, the clinical association between Tid1 expression and progression of HNSCC was explored. It was found that expression of Tid1 was negatively associated with tumour status, recurrence, and survival prognosis using immunohistochemical analysis of primary HNSCC patient tumour tissue. Secondly, ectopic expression of Tid1 in HNSCC cells was shown to significantly inhibit cell proliferation, migration, invasion, anchorage-independent growth, and xenotransplantation tumourigenicity. Thirdly, we showed that overexpression of Tid1 attenuated EGFR activity and blocked the activation of AKT in HNSCC cells, which are known to be involved in the regulation of survival in HNSCC cells. On the other hand, ectopic expression of constitutively active AKT greatly reduced apoptosis induced by Tid1 overexpression. Together, these findings suggest that Tid1 functions as a tumour suppressor in HNSCC tumourigenesis.
Insights
Tumourous imaginal disc 1 (Tid1) acts as a tumor suppressor in head and neck squamous cell carcinoma (HNSCC). Tid1 inhibits HNSCC progression, migration, and survival by attenuating EGFR and AKT signaling pathways.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Tumourous imaginal disc 1 (Tid1) is a human homologue of Drosophila Tid56, implicated in key cellular processes.
- Tid1 plays a role in intracellular signaling pathways regulating apoptosis, cell proliferation, and cell survival.
- Head and neck squamous cell carcinoma (HNSCC) is a complex malignancy with significant unmet therapeutic needs.
Purpose of the Study:
- To investigate the anti-tumourigenic activity of Tid1 in HNSCC.
- To explore the clinical association between Tid1 expression and HNSCC progression.
- To elucidate the molecular mechanisms underlying Tid1's function in HNSCC.
Main Methods:
- Immunohistochemical analysis of Tid1 expression in primary HNSCC patient tumor tissues.
- In vitro studies involving ectopic expression of Tid1 in HNSCC cell lines.
- In vivo xenotransplantation models to assess tumourigenicity.
- Western blot analysis to evaluate EGFR and AKT signaling pathway activation.
Main Results:
- Tid1 expression negatively correlated with HNSCC tumor status, recurrence, and patient survival prognosis.
- Ectopic Tid1 expression significantly inhibited HNSCC cell proliferation, migration, invasion, and anchorage-independent growth.
- Tid1 overexpression attenuated EGFR activity and blocked AKT activation in HNSCC cells.
- Overexpression of constitutively active AKT partially rescued apoptosis induced by Tid1.
Conclusions:
- Tid1 functions as a tumor suppressor in head and neck squamous cell carcinoma.
- Tid1 inhibits HNSCC progression and tumorigenesis through the EGFR/AKT signaling pathway.
- Tid1 represents a potential therapeutic target for HNSCC treatment.
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