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Antitumor activity in colorectal cancer induced by hinokiflavone
Jing Zhou1,2, Rongce Zhao3, Tinghong Ye4
1Department of Medical Oncology, Cancer Center, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China.
Background And Aim:
Colorectal cancer is one of the most common malignant disease worldwide with highly metastatic potential. Identification of effective therapeutic treatment overcoming such disease is an urgent need. Our study focuses on hinokiflavone as an antitumor agent against colorectal cancer.
Methods:
MTT assay, cell colony formation assay, Hoechst staining, flow cytometry, Western blot analysis, real-time polymerase chain reaction, and migration and invasion assay were performed to identify the effects of hinokiflavone on cell proliferation, apoptosis, and metastasis. CT26 tumor-bearing mice model was conducted to explore the antitumor activity of hinokiflavone in vivo. Immunohistochemistry staining was used to detect the protein expression of Ki-67, cleaved caspase-3, and MMP9 in treated tumors. Acute toxicity was evaluated by serological and hematological analyses, and drug side effect on organs was evaluated by hematoxylin and eosin staining.
Results:
Hinokiflavone reduced the proliferation, migration, and invasion and promoted the apoptosis in colorectal tumor cells in vitro. Treatment of hinokiflavone at a tolerable and safe dose (50 mg/kg) significantly suppressed tumor growth in mice bearing CT26 tumors by reducing tumor proliferation and metastasis and inducing apoptosis. Mechanically, treatment of hinokiflavone induced apoptosis by loss of mitochondrial transmembrane potential and increased reactive oxygen species generation.
Conclusions:
Hinokiflavone suppressed colorectal tumor cell proliferation, induced apoptosis via the reactive oxygen species-mitochondria-mediated apoptotic pathway, and inhibited tumor cell migration and invasion. Antitumor activity of hinokiflavone was also validated in mice model without observed toxicity. Our findings suggested that the plant-derived hinokiflavone could be used as an antitumor agent against colorectal cancer.
Insights
Hinokiflavone, a plant-derived compound, effectively inhibits colorectal cancer growth by reducing proliferation and metastasis while promoting apoptosis. This natural agent demonstrated significant antitumor activity in mice without toxicity, suggesting its potential as a therapeutic option.
Area of Science:
- Oncology
- Pharmacology
- Natural Products
Background:
- Colorectal cancer (CRC) is a prevalent malignancy with high metastatic potential.
- There is an urgent need for novel therapeutic strategies to combat CRC.
- Hinokiflavone is explored as a potential antitumor agent against CRC.
Purpose of the Study:
- To investigate the antitumor effects of hinokiflavone on colorectal cancer cells in vitro and in vivo.
- To elucidate the mechanisms underlying hinokiflavone's anti-cancer activity.
- To assess the safety and efficacy of hinokiflavone as a potential CRC therapeutic.
Main Methods:
- In vitro assays: MTT, colony formation, Hoechst staining, flow cytometry, Western blot, real-time PCR, migration/invasion assays.
- In vivo study: CT26 tumor-bearing mice model with immunohistochemistry for Ki-67, cleaved caspase-3, MMP9.
- Toxicity assessment: serological, hematological analyses, and H&E staining.
Main Results:
- Hinokiflavone suppressed colorectal cancer cell proliferation, migration, and invasion, while inducing apoptosis in vitro.
- A safe dose (50 mg/kg) of hinokiflavone significantly inhibited tumor growth, proliferation, and metastasis in vivo.
- Mechanistically, hinokiflavone induced apoptosis through loss of mitochondrial potential and increased reactive oxygen species (ROS).
Conclusions:
- Hinokiflavone exhibits potent anti-colorectal cancer activity by inhibiting proliferation, inducing apoptosis via ROS-mitochondria pathway, and suppressing migration/invasion.
- The antitumor effects were validated in a preclinical mouse model with no observed toxicity.
- Plant-derived hinokiflavone shows promise as a natural antitumor agent for colorectal cancer treatment.
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