[학위논문]대장암세포에서 Akt/mTOR/p53 신호경로 조절을 통한 녹나무 추출물의 G1 세포주기 정지 유도 효과 Extracts from Cinnamomum camphora induce G1 Cell Cycle Arrest in Colon carcinoma cell by its Regulation of Akt/mTOR/p53 signaling Pathway원문보기
The Cinnamomum camphora, a plant native to Korea, China and Japan, is known as a traditional medicine for chest congestion and inflammation related disease. lately, some studies have been reported that Cinnamomum camphora extract (CCE) involved in anti-cancer effects. Despite recent attention, mecha...
The Cinnamomum camphora, a plant native to Korea, China and Japan, is known as a traditional medicine for chest congestion and inflammation related disease. lately, some studies have been reported that Cinnamomum camphora extract (CCE) involved in anti-cancer effects. Despite recent attention, mechanisms of anticancer effect triggered by CCE are not understood precisely. To end this, we investigated cell cycle arrest effect of CCE on HCT116 colon cancer cells and examined the molecular mechanisms of it. The results of an MTT assay and Wound healing assay demonstrated that CCE decreasing HCT116 viability and mobility. also, cell cycle arrest, assessed by PI staining, were occurred at G1 phase by the treatment of CCE. Akt is the serine-threonine kinase which plays crucial role in broadly influential signaling pathway. It controls Mammalian Target of Rapamycin (mTOR) and its cascade is associated with survival of cancer. We confirmed the expression of cell cycle associated molecules, including p53, p21, cyclin E, CDK2 and its upstream signal molecular. Moreover, the treatment of Akt inhibitor (LY294002), mTOR inhibitor (Rapamycin), p53 inhibitor (Pifithrin-α) showed that the G1 cell cycle arrest occurred through the regulation of Akt/mTOR-dependent pathway and p53-independent pathway. Altogether, our results suggest that extracts of CCE have anti-cancer effects against HCT116 human colorectal carcinoma cells via modulation of Akt/mTOR signaling pathway, also in p53-independent pathway.
The Cinnamomum camphora, a plant native to Korea, China and Japan, is known as a traditional medicine for chest congestion and inflammation related disease. lately, some studies have been reported that Cinnamomum camphora extract (CCE) involved in anti-cancer effects. Despite recent attention, mechanisms of anticancer effect triggered by CCE are not understood precisely. To end this, we investigated cell cycle arrest effect of CCE on HCT116 colon cancer cells and examined the molecular mechanisms of it. The results of an MTT assay and Wound healing assay demonstrated that CCE decreasing HCT116 viability and mobility. also, cell cycle arrest, assessed by PI staining, were occurred at G1 phase by the treatment of CCE. Akt is the serine-threonine kinase which plays crucial role in broadly influential signaling pathway. It controls Mammalian Target of Rapamycin (mTOR) and its cascade is associated with survival of cancer. We confirmed the expression of cell cycle associated molecules, including p53, p21, cyclin E, CDK2 and its upstream signal molecular. Moreover, the treatment of Akt inhibitor (LY294002), mTOR inhibitor (Rapamycin), p53 inhibitor (Pifithrin-α) showed that the G1 cell cycle arrest occurred through the regulation of Akt/mTOR-dependent pathway and p53-independent pathway. Altogether, our results suggest that extracts of CCE have anti-cancer effects against HCT116 human colorectal carcinoma cells via modulation of Akt/mTOR signaling pathway, also in p53-independent pathway.
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