| ▲ The mechanism of prostate cancer proliferation and treatment resistance by ‘FOXA1‘ gene mutation has been revealed. (Photo = DB) |
[메디컬투데이=이승재 기자] The mechanism of prostate cancer proliferation and treatment resistance by ‘FOXA1’ gene mutation has been revealed.
The findings of mouse experimental studies that investigated the mechanism of FOXA1 gene mutations involved in tumor growth and treatment resistance were published in Science.
In the West, prostate cancer has the highest frequency of cancer in men, and the frequency of occurrence is increasing in Korea.
The causes of prostate cancer include age, race, and family history, and fundamentally, it grows under the influence of male hormones.
Hormone therapy, targeting such male hormones is the core of prostate cancer treatment. Hormonal therapy is effective in the early days, but it is often resistant, and in this case, treatment becomes more difficult.
Researchers at the University of Michigan Rogel Health Cancer Center in the United States used a mouse model to understand the mechanism of mutations in the mutation of the company’s Foxa1, which is involved in the growth and treatment resistance of prostate cancer.
‘FOXA1’ is a transcription factor that promotes the combination of Androgen receptors to DNA, and is mutated at 10-40%of patients with hormone dependent prostate cancer.
As a result of the study, the first group mutation, commonly observed in primary prostate cancer, appeared with the loss of the ‘TP53’ gene, and the FOXA1 and TP53 mutations worked together to aggressively promote tumor growth.
In addition, class 2 mutations, commonly observed in metastatic prostate cancer, have been replaced with the identity of the cell system, rather than independently triggered tumor growth, allowing cancer cells to resistant to hormone treatment.
The researchers concluded that the FOXA1 gene showed two mutations, which resulted in cancer growth and therapeutic resistance.
Reporter Lee Seung -jae (eCCTHOMAS@mdtoday.co.kr)
[저작권자ⓒ 메디컬투데이. 무단전재-재배포 금지]
