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DDX5 Functions as a Tumor Suppressor in Tongue Cancer
Qingqing Liu1, Yangqing Sun1, Min Long2
1Department of Oncology, Xiangya Hospital, Central South University, Changsha 410008, China.
Abstract:
DEAD-box polypeptide 5 (DDX5), a DEAD-box RNA helicase, is a multifunctional protein that plays important roles in many physiological and pathological processes. Contrary to its documented oncogenic role in a wide array of cancers, we herein demonstrate that DDX5 serves as a tumor suppressor in tongue cancer. The high expression of DDX5 is correlated with better prognosis for clinical tongue cancer patients. DDX5 downregulates the genes associated with tongue cancer progression. The knockdown of DDX5 promotes, while the overexpression of DDX5 inhibits, tongue cancer proliferation, development, and cisplatin resistance. Furthermore, the expression of DDX5 in tongue cancer is associated with immune cell infiltration in the tumor microenvironment. Specifically, the expression of DDX5 is associated with the reduced infiltration of M2 macrophages and increased infiltration of T cell clusters, which may contribute to anticancer effects in the tumor microenvironment. In this study, we establish DDX5 as a valuable prognostic biomarker and an important tumor suppressor in tongue cancer.
Insights
DEAD-box polypeptide 5 (DDX5) acts as a tumor suppressor in tongue cancer, contrary to its role in other cancers. High DDX5 expression correlates with better patient prognosis and inhibits cancer progression.
Area of Science:
- Oncology
- Molecular Biology
- Immunology
Background:
- DEAD-box polypeptide 5 (DDX5) is a multifunctional RNA helicase implicated in various cellular processes.
- DDX5 is recognized for its oncogenic functions in numerous cancer types.
- Its role in tongue cancer, however, remained largely unexplored.
Purpose of the Study:
- To investigate the role of DDX5 in tongue cancer.
- To determine DDX5's prognostic value in tongue cancer patients.
- To elucidate the mechanisms underlying DDX5's function in tongue cancer progression and the tumor microenvironment.
Main Methods:
- Analysis of DDX5 expression levels in clinical tongue cancer samples.
- Correlation of DDX5 expression with patient prognosis and clinicopathological features.
- In vitro experiments involving DDX5 knockdown and overexpression to assess effects on cancer cell proliferation, development, and cisplatin resistance.
- Investigation of DDX5 expression's association with immune cell infiltration within the tumor microenvironment.
Main Results:
- High DDX5 expression is significantly correlated with improved prognosis in tongue cancer patients.
- DDX5 downregulation promotes tongue cancer proliferation, development, and cisplatin resistance.
- DDX5 overexpression inhibits these processes.
- DDX5 expression is linked to reduced M2 macrophage infiltration and increased T cell cluster infiltration in the tumor microenvironment.
Conclusions:
- DDX5 functions as a tumor suppressor in tongue cancer, contradicting its established oncogenic role in other malignancies.
- DDX5 serves as a valuable prognostic biomarker for tongue cancer.
- Modulation of DDX5 expression impacts tongue cancer progression and the tumor immune microenvironment, suggesting therapeutic potential.
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