Discover oncology · 2025
Anticancer role of Gramicidin A in myeloid leukemia.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Maham Syeda, Khan Mudassir, Noor Aleeha, Adnan Fazal, Kakar Salik Javed, Mian Afsar Ali, Khan Dilawar
Аннотация
BACKGROUND: Myeloid and lymphoid progenitor cells can develop leukemia. Acute myeloid leukemia (AML) and chronic myeloid leukemia (CML) are two types of myeloid leukemia, depending on how the disease progresses. Acute promyelocytic leukemia (APL) a subtype of AML and CML were the main subjects of this investigation. Despite the encouraging results of FDA-approved therapies, there is still relapse and no cure. Although it has recently been demonstrated that the well-known antibiotic gramicidin A (GA) inhibits the growth of tumor cells, the mechanism of action have not been investigated in leukemia.
METHODS: This study used pharmacological and biochemical approaches to investigate anticancer potential and mechanism of action of GA in APL and CML.
RESULTS: We report that, irrespective of apoptosis induction, GA inhibits the proliferative potential of APL and CML cell lines (p < 0.05 and p < 0.0001). GA down regulate expression of AXL-RTK and EYA3 genes which are regulators of Wnt/β-catenin pathway. Furthermore we showed that Wnt/β-catenin target genes including c-Myc and Axin2 were down regulated which were also linked to the additive anticancer effect of GA in combination with Imatinib for CML and ATRA for APL (p < 0.0001). Moreover, hemolysis of red blood cell (RBCs) was not induced by any inhibitory concentration of GA.
CONCLUSION: According to our findings, GA significantly reduces the leukemogenic potential of APL and CML without causing any hemolysis in RBCs, indicating its safety profile with respect to red blood cell integrity, and may eventually be a viable substitute/candidate for therapeutic intervention in APL and CML.
METHODS: This study used pharmacological and biochemical approaches to investigate anticancer potential and mechanism of action of GA in APL and CML.
RESULTS: We report that, irrespective of apoptosis induction, GA inhibits the proliferative potential of APL and CML cell lines (p < 0.05 and p < 0.0001). GA down regulate expression of AXL-RTK and EYA3 genes which are regulators of Wnt/β-catenin pathway. Furthermore we showed that Wnt/β-catenin target genes including c-Myc and Axin2 were down regulated which were also linked to the additive anticancer effect of GA in combination with Imatinib for CML and ATRA for APL (p < 0.0001). Moreover, hemolysis of red blood cell (RBCs) was not induced by any inhibitory concentration of GA.
CONCLUSION: According to our findings, GA significantly reduces the leukemogenic potential of APL and CML without causing any hemolysis in RBCs, indicating its safety profile with respect to red blood cell integrity, and may eventually be a viable substitute/candidate for therapeutic intervention in APL and CML.