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Expression of TAp73α affects the therapy effect of chemotherapy drugs in gastric cancer
- Source :
- Oncology research.
- Publication Year :
- 2018
-
Abstract
- The transcription factor TAp73, a transcriptionally active isoform of p73, has high structure and function similaritieswith its homolog p53, therefore, are thought to be a cancer therapy candidate target. However, there is still a controversy about the tumor suppressor role of TAp73, since it has been found in numerous studies that TAp73 expression is elevated in different cancers. Thus, we take effort to clarify the influence of TAp73 on gastric cancer (GC) chemotherapy. Multiple cell lines of GC such as SNU-1, SNU-3, and AGS were applied to investigate expression of TAp73. Flow cytometry was utilized to detect apoptosis, revealing how TAp73 overexpression affected anticancer drug (ACD). Additionally, we explored how TAp73 overexpression influenced apoptotic cells of neoplastic tissues and tumor size of nude mice in vivo. Our results indicated that TAp73 was down-regulated in GC cells after chemotherapy drugs treatment. Besides, enforced expression of TAp73 affects chemotherapeutic drugs induced GC cell apoptosis, which is dependent on p53. The expression of TAp73 was regulated by its transcription factor, E2F1, in response to chemotherapy drugs. Our in vivo xenograft results also suggested that transfection of TAp73 affects the tumor suppression effect of 5-FU. Consequently, the findings of our study demonstrate that E2F1 and TAp73α are oncogenic and throw light upon the underlying mechanism of their role against apoptosis.
- Subjects :
- 0301 basic medicine
Cancer Research
Chemotherapy
medicine.diagnostic_test
business.industry
medicine.medical_treatment
Cancer
General Medicine
Transfection
medicine.disease
Flow cytometry
03 medical and health sciences
030104 developmental biology
0302 clinical medicine
Oncology
In vivo
Apoptosis
030220 oncology & carcinogenesis
Cancer research
Medicine
E2F1
business
Transcription factor
Subjects
Details
- ISSN :
- 15553906
- Database :
- OpenAIRE
- Journal :
- Oncology research
- Accession number :
- edsair.doi.dedup.....7434a0763c3e565f30eeb39460e08333