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Published on: August 23, 2019
Naringin inhibits thyroid cancer cell proliferation and induces cell apoptosis through repressing PI3K/AKT pathway
Jun Zhou1, Liang Xia1, Yu Zhang2
1Department of Nuclear Medicine, Wuhan Central Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430014, China.
Abstract:
The present study aimed to investigate the anti-tumor effects of naringin in thyroid cancer (TC), and to explore the underlying mechanisms. TC cell lines TPC-1 and SW1736 were treated with 6, 12 or 25 μg/ml naringin for indicated times. Then, cell proliferation was determined using 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay, and cell apoptosis was analyzed by flow cytometer. Moreover, cell proliferation and apoptosis related genes (cyclin D1, c-Myc, survivin, Caspase3, Bcl-2, and Bax) were measured by western blot assay and quantitative reverse transcription-polymerase chain reaction (qRT-PCR) respectively. Cleaved Caspase3 was measured using western blot assay. Phosphatidylinositol 3-kinase (PI3K)/AKT pathway was also analyzed in this study. Results indicated that naringin dose- and time-dependently inhibited TPC-1 and SW1736 cell proliferation, and naringin dose-dependently induced TPC-1 and SW1736 cell apoptosis. In addition, we found that naringin dose-dependently enhanced the expression of Caspase3, cleaved Caspase3 and Bax, and reduced the expression of cyclin D1, c-Myc, survivin, and Bcl-2 in TPC-1 and SW1736 cells. Moreover, we found that naringin dose-dependently suppressed PI3K/AKT pathway activation in TC cells. In conclusion, the data of this study suggested that naringin presented anti-tumor effects in TC cells through inhibiting TC cell proliferation and inducing cell apoptosis via regulating the expression of cell proliferation and apoptosis related genes and PI3K/AKT pathway activation. Our study suggested the potential value of naringin in the treatment of TC and provided more theoretical evidence for the treatment of TC.
Insights
Naringin exhibits anti-tumor properties against thyroid cancer (TC) by inhibiting cell proliferation and inducing apoptosis. It modulates key genes and the PI3K/AKT pathway, suggesting potential therapeutic value for TC treatment.
Area of Science:
- Biochemistry
- Molecular Biology
- Oncology
Background:
- Thyroid cancer (TC) remains a significant health concern with ongoing research for novel therapeutic agents.
- Naringin, a natural flavonoid, has demonstrated various biological activities, prompting investigation into its anti-cancer potential.
Purpose of the Study:
- To investigate the anti-tumor effects of naringin in thyroid cancer (TC) cell lines.
- To elucidate the underlying molecular mechanisms, including effects on cell proliferation, apoptosis, and signaling pathways.
Main Methods:
- Thyroid cancer cell lines (TPC-1 and SW1736) were treated with varying concentrations of naringin.
- Cell proliferation was assessed using MTT assay; apoptosis was analyzed by flow cytometry.
- Gene expression related to proliferation and apoptosis (cyclin D1, c-Myc, survivin, Caspase3, Bcl-2, Bax) was measured by qRT-PCR and Western blot.
- PI3K/AKT pathway activation was also analyzed.
Main Results:
- Naringin significantly inhibited TC cell proliferation and induced apoptosis in a dose- and time-dependent manner.
- Naringin modulated the expression of key apoptosis-related genes, increasing Bax, Caspase3, and cleaved Caspase3, while decreasing cyclin D1, c-Myc, survivin, and Bcl-2.
- Naringin suppressed the activation of the PI3K/AKT signaling pathway in TC cells.
Conclusions:
- Naringin demonstrates potent anti-tumor effects against thyroid cancer cells.
- These effects are mediated by the inhibition of cell proliferation, induction of apoptosis, regulation of specific genes, and suppression of the PI3K/AKT pathway.
- Naringin shows promise as a potential therapeutic agent for thyroid cancer, warranting further investigation.
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