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TP73, an under-appreciated player in non-Hodgkin lymphoma pathogenesis and management
H M Hassan, B J Dave, R K Singh1
1Munroe Meyer Institute for Genetics and Rehabilitation, University of Nebraska Medical Center, 985440 Nebraska Medical Center, Omaha, NE 68198-5440, USA. bdave@unmc.edu.
Abstract:
The TP73 gene is a member of the TP53 family with high structural homology to p53 and capable of transactivating p53 target genes. The TP73 gene locus which is highly conserved and complex, encodes for two classes of isoforms TAp73 (tumor suppressor isoforms containing the transactivation domain) and ΔNp73 (oncogenic isoforms, truncated and lacking the transactivation domain) with opposing effects. The balance between TAp73 and ΔNp73 isoforms and their harmony with other members of the TP73 family regulate various cellular responses such as apoptosis, autophagy, proliferation, and differentiation. The transcriptionally active isoforms of p73 are capable of inducing apoptosis in cancer cells independent of p53 status. Unlike p53, p73 is rarely mutated in cancers, however, the ratio of ΔNp73:TAp73 is frequently up-regulated in many carcinomas and is indicative of poor prognosis. Moreover, p73 is an important determinant of chemosensitivity and radiosensitivity, the two major treatment modalities for lymphoma. In the current review, we will provide an overview of recent progress discussing the role of TP73 in cancer, specifically addressing its relevance to lymphomagenesis, progression, therapy resistance, and its potential as a novel therapeutic target.
Insights
The TP73 gene, encoding tumor suppressor and oncogenic isoforms, plays a critical role in cancer. Its dysregulation, particularly the ΔNp73:TAp73 ratio, impacts lymphoma development and treatment resistance, highlighting its therapeutic potential.
Area of Science:
- Molecular biology
- Cancer genetics
- Tumor suppressor genes
Background:
- TP73 gene encodes TAp73 (tumor suppressor) and ΔNp73 (oncogenic) isoforms with opposing cellular functions.
- TP73 is structurally homologous to TP53 and regulates apoptosis, autophagy, proliferation, and differentiation.
- Unlike TP53, TP73 is rarely mutated in cancers, but its isoform balance is crucial.
Purpose of the Study:
- To review the role of the TP73 gene in cancer, focusing on its involvement in lymphomagenesis.
- To discuss TP73's relevance in lymphoma progression and therapy resistance.
- To explore the potential of TP73 as a novel therapeutic target in cancer treatment.
Main Methods:
- Literature review of recent progress on TP73 gene function in cancer.
- Analysis of TP73 isoform balance (ΔNp73:TAp73 ratio) in various carcinomas.
- Examination of TP73's impact on chemosensitivity and radiosensitivity in lymphoma.
Main Results:
- The ratio of ΔNp73:TAp73 is frequently up-regulated in carcinomas, correlating with poor prognosis.
- TP73 isoforms influence apoptosis, autophagy, proliferation, and differentiation.
- p73 is a key determinant of chemosensitivity and radiosensitivity in lymphoma treatment.
Conclusions:
- TP73 dysregulation, specifically the ΔNp73:TAp73 ratio, is implicated in lymphomagenesis and progression.
- TP73 influences therapeutic response, making it a potential target for overcoming resistance.
- Targeting TP73 offers a promising strategy for novel cancer therapies, particularly in lymphoma.
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