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β-asarone inhibited cell growth and promoted autophagy via P53/Bcl-2/Bclin-1 and P53/AMPK/mTOR pathways in Human Glioma U251 cells.
J Cell Physiol 2018; 233(3):2434-2443JC

Abstract

Glioma is the most common type of primary brain tumor and has an undesirable prognosis. Autophagy plays an important role in cancer therapy, but it is effect is still not definite. P53 is an important tumor suppressor gene and protein that is closely to autophagy. Our aim was to study the effect of β-asarone on inhibiting cell proliferation in human glioma U251 cells and to detect the effect of the inhibition on autophagy through the P53 signal pathway. For cell growth, the cells were divided into four groups: the model, β-asarone, temozolomide (TMZ), and co-administration groups. For cell autoghapy and the P53 pathway, the cells were divided into six groups: the model, β-asarone, 3MA, Rapa, Pifithrin-µ, and NSC groups. The counting Kit-8 assay and flow cytometry (FCM) were then used to measure the cell proliferation and cycle. Electron microscopy was used to observe autophagosome formation. Cell immunohistochemistry/-immunofluorescence, FCM and Western blot (WB) were used to examine the expression of Beclin-1 and P53. The levels of P53 and GAPDH mRNA were detected by RT-PCR. Using WB, we determined autophagy-related proteins Beclin-1, LC3-II/I, and P62 and those of the P53 pathway-related proteins P53, Bcl-2, mTOR, P-mTOR, AMPK, P-AMPK, and GAPDH. We got the results that β-asarone changed the cellular morphology, inhibited cell proliferation, and enhanced the expression of P53, LC3-II/I, Beclin-1, AMPK, and pAMPK while inhibiting the expression of P62, Bcl-2, mTOR, and pmTOR. All the data suggested that β-asarone could reduce the cell proliferation and promote autophagy possible via the P53 pathway in U251 cells.

Authors+Show Affiliations

Guangzhou University of Chinese Medicine, Guangzhou, P.R. China.Guangzhou University of Chinese Medicine, Guangzhou, P.R. China.Guangzhou University of Chinese Medicine, Guangzhou, P.R. China.Guangzhou University of Chinese Medicine, Guangzhou, P.R. China.The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, P.R. China.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

28776671

Citation

Wang, Nanbu, et al. "Β-asarone Inhibited Cell Growth and Promoted Autophagy Via P53/Bcl-2/Bclin-1 and P53/AMPK/mTOR Pathways in Human Glioma U251 Cells." Journal of Cellular Physiology, vol. 233, no. 3, 2018, pp. 2434-2443.
Wang N, Zhang Q, Luo L, et al. Β-asarone inhibited cell growth and promoted autophagy via P53/Bcl-2/Bclin-1 and P53/AMPK/mTOR pathways in Human Glioma U251 cells. J Cell Physiol. 2018;233(3):2434-2443.
Wang, N., Zhang, Q., Luo, L., Ning, B., & Fang, Y. (2018). Β-asarone inhibited cell growth and promoted autophagy via P53/Bcl-2/Bclin-1 and P53/AMPK/mTOR pathways in Human Glioma U251 cells. Journal of Cellular Physiology, 233(3), pp. 2434-2443. doi:10.1002/jcp.26118.
Wang N, et al. Β-asarone Inhibited Cell Growth and Promoted Autophagy Via P53/Bcl-2/Bclin-1 and P53/AMPK/mTOR Pathways in Human Glioma U251 Cells. J Cell Physiol. 2018;233(3):2434-2443. PubMed PMID: 28776671.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - β-asarone inhibited cell growth and promoted autophagy via P53/Bcl-2/Bclin-1 and P53/AMPK/mTOR pathways in Human Glioma U251 cells. AU - Wang,Nanbu, AU - Zhang,Qinxin, AU - Luo,Laiyu, AU - Ning,Baile, AU - Fang,Yongqi, Y1 - 2017/08/30/ PY - 2017/06/21/received PY - 2017/08/01/accepted PY - 2017/8/5/pubmed PY - 2017/12/13/medline PY - 2017/8/5/entrez KW - U251 KW - autophagy KW - glioma KW - p53 KW - β-asarone SP - 2434 EP - 2443 JF - Journal of cellular physiology JO - J. Cell. Physiol. VL - 233 IS - 3 N2 - Glioma is the most common type of primary brain tumor and has an undesirable prognosis. Autophagy plays an important role in cancer therapy, but it is effect is still not definite. P53 is an important tumor suppressor gene and protein that is closely to autophagy. Our aim was to study the effect of β-asarone on inhibiting cell proliferation in human glioma U251 cells and to detect the effect of the inhibition on autophagy through the P53 signal pathway. For cell growth, the cells were divided into four groups: the model, β-asarone, temozolomide (TMZ), and co-administration groups. For cell autoghapy and the P53 pathway, the cells were divided into six groups: the model, β-asarone, 3MA, Rapa, Pifithrin-µ, and NSC groups. The counting Kit-8 assay and flow cytometry (FCM) were then used to measure the cell proliferation and cycle. Electron microscopy was used to observe autophagosome formation. Cell immunohistochemistry/-immunofluorescence, FCM and Western blot (WB) were used to examine the expression of Beclin-1 and P53. The levels of P53 and GAPDH mRNA were detected by RT-PCR. Using WB, we determined autophagy-related proteins Beclin-1, LC3-II/I, and P62 and those of the P53 pathway-related proteins P53, Bcl-2, mTOR, P-mTOR, AMPK, P-AMPK, and GAPDH. We got the results that β-asarone changed the cellular morphology, inhibited cell proliferation, and enhanced the expression of P53, LC3-II/I, Beclin-1, AMPK, and pAMPK while inhibiting the expression of P62, Bcl-2, mTOR, and pmTOR. All the data suggested that β-asarone could reduce the cell proliferation and promote autophagy possible via the P53 pathway in U251 cells. SN - 1097-4652 UR - https://www.unboundmedicine.com/medline/citation/28776671/β_asarone_inhibited_cell_growth_and_promoted_autophagy_via_P53/Bcl_2/Bclin_1_and_P53/AMPK/mTOR_pathways_in_Human_Glioma_U251_cells_ L2 - https://doi.org/10.1002/jcp.26118 DB - PRIME DP - Unbound Medicine ER -