Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
[Cephaeline attenuates malignant biological behaviors of colorectal cancer by regulating the Ras signaling pathway].
Аннотация на английскомСтатьяНазвание 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.
Han Liang, Li Baichao, Wang Bingzhe, Zhang Zhiwei, Zhang Jiuna
Аннотация
OBJECTIVES: To investigate the mechanism of cephaeline for suppressing malignant biological behaviors of colorectal cancer (CRC).
METHODS: Network pharmacology was employed to identify the core targets and signaling pathways of cephaeline in CRC treatment. The binding between the key targets of CRC and cephaeline was simulated using molecular docking. CCK-8 assay was used to assess the viability of HCT116 and DLD-1 cells treated with 2-32 nmol/L cephaeline for 24, 48, and 72 h to determine the optimal treatment condition. The effects of cephaeline treatments (at 2 and 4 nmol/L in HCT116 cells and at 4 and 8 nmol/L in DLD-1 cells) for 48 h on cell proliferation, migration, invasion, epithelial‑mesenchymal transition (EMT), apoptosis, and expressions of RAS signaling pathway proteins were evaluated using colony-forming assay, wound healing assay, Transwell assays, and Western blotting.
RESULTS: Network pharmacology analysis suggested that cephaeline inhibited CRC mainly by regulating the targets such as MAPK, VEGFA, and PDGFRB and modulating the Rap1, Ras, cAMP, and PI3K-Akt signaling pathways. Molecular docking results showed that the binding energies of cephaeline with PDGFRB and MAPK1 were less than -5 kcal/mol, indicating spontaneous and stable binding between them. In HCT116 and DLD-1 cells, treatment with cephaeline concentration-dependently suppressed the cell viability, proliferation, migration, and invasion, downregulated the expressions of PCNA, MMP9, VEGF-C, BCL-2, N-cadherin, vimentin, VEGF-A, PDGFRB, MYC, and MAPK1, and upregulated the expression levels of E-cadherin and BAX.
CONCLUSIONS: Cephaeline suppresses malignant biological behaviors of CRC possibly by regulating the RAS signaling pathway.
METHODS: Network pharmacology was employed to identify the core targets and signaling pathways of cephaeline in CRC treatment. The binding between the key targets of CRC and cephaeline was simulated using molecular docking. CCK-8 assay was used to assess the viability of HCT116 and DLD-1 cells treated with 2-32 nmol/L cephaeline for 24, 48, and 72 h to determine the optimal treatment condition. The effects of cephaeline treatments (at 2 and 4 nmol/L in HCT116 cells and at 4 and 8 nmol/L in DLD-1 cells) for 48 h on cell proliferation, migration, invasion, epithelial‑mesenchymal transition (EMT), apoptosis, and expressions of RAS signaling pathway proteins were evaluated using colony-forming assay, wound healing assay, Transwell assays, and Western blotting.
RESULTS: Network pharmacology analysis suggested that cephaeline inhibited CRC mainly by regulating the targets such as MAPK, VEGFA, and PDGFRB and modulating the Rap1, Ras, cAMP, and PI3K-Akt signaling pathways. Molecular docking results showed that the binding energies of cephaeline with PDGFRB and MAPK1 were less than -5 kcal/mol, indicating spontaneous and stable binding between them. In HCT116 and DLD-1 cells, treatment with cephaeline concentration-dependently suppressed the cell viability, proliferation, migration, and invasion, downregulated the expressions of PCNA, MMP9, VEGF-C, BCL-2, N-cadherin, vimentin, VEGF-A, PDGFRB, MYC, and MAPK1, and upregulated the expression levels of E-cadherin and BAX.
CONCLUSIONS: Cephaeline suppresses malignant biological behaviors of CRC possibly by regulating the RAS signaling pathway.