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[Molecular mechanism of ophiopogonin B induced cellular autophagy of human cervical cancer HeLa cells].
Yao Xue Xue Bao 2013; 48(6):855-9YX

Abstract

This study is to investigate the antitumor activity of ophiopogonin B (OP-B). MTT assay, flow cytometric analysis, acridine orange staining, Lyso-Tracker Red staining and HeLa-GFP-LC3 transfect cells assay were used to detect the proliferation activity, apoptosis and autophagy of HeLa cells. The results showed that OP-B exerted potent antiproliferative activity on HeLa cells, the cell growth inhibition effect of OP-B was not due to apoptosis and OP-B could induce autophagy of HeLa cells. OP-B also induced the protein expression up-regulation of Beclin-1 and promoted LC3 I transformation LC3 II, which were representative proteins of autophagy. Furthermore, 3-MA, an inhibitor of autophagy, not only inhibited OP-B-mediated autophagy but also almost completely reversed the antiproliferative effect of OP-B, suggesting that the growth inhibition effect of OP-B was autophagy dependent. Western blotting demonstrated that OP-B inhibited the phosphorylation of Akt and its' downstream vital protein, such as mTOR and p70S6K. In addition, OP-B also induced the protein expression up-regulation of PTEN, which is a negative regulation protein for Akt/mTOR signaling pathway. However, OP-B did not affect the protein expression of total Akt. Collectively, the antitumor effects of OP-B were autophagy-dependent via repression Akt/mTOR signaling pathway. Therefore, OP-B is a prospective inhibitor of Akt/mTOR and may be used as an alternative compound to treat cervical carcinoma.

Authors+Show Affiliations

Institute of Chemical Biology, Henan University, Kaifeng 475004, China.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

chi

PubMed ID

23984518

Citation

Xu, Qiu-Ju, et al. "[Molecular Mechanism of Ophiopogonin B Induced Cellular Autophagy of Human Cervical Cancer HeLa Cells]." Yao Xue Xue Bao = Acta Pharmaceutica Sinica, vol. 48, no. 6, 2013, pp. 855-9.
Xu QJ, Hou LL, Hu GQ, et al. [Molecular mechanism of ophiopogonin B induced cellular autophagy of human cervical cancer HeLa cells]. Yao Xue Xue Bao. 2013;48(6):855-9.
Xu, Q. J., Hou, L. L., Hu, G. Q., & Xie, S. Q. (2013). [Molecular mechanism of ophiopogonin B induced cellular autophagy of human cervical cancer HeLa cells]. Yao Xue Xue Bao = Acta Pharmaceutica Sinica, 48(6), pp. 855-9.
Xu QJ, et al. [Molecular Mechanism of Ophiopogonin B Induced Cellular Autophagy of Human Cervical Cancer HeLa Cells]. Yao Xue Xue Bao. 2013;48(6):855-9. PubMed PMID: 23984518.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Molecular mechanism of ophiopogonin B induced cellular autophagy of human cervical cancer HeLa cells]. AU - Xu,Qiu-Ju, AU - Hou,Li-Li, AU - Hu,Guo-Qiang, AU - Xie,Song-Qiang, PY - 2013/8/30/entrez PY - 2013/8/30/pubmed PY - 2016/1/26/medline SP - 855 EP - 9 JF - Yao xue xue bao = Acta pharmaceutica Sinica JO - Yao Xue Xue Bao VL - 48 IS - 6 N2 - This study is to investigate the antitumor activity of ophiopogonin B (OP-B). MTT assay, flow cytometric analysis, acridine orange staining, Lyso-Tracker Red staining and HeLa-GFP-LC3 transfect cells assay were used to detect the proliferation activity, apoptosis and autophagy of HeLa cells. The results showed that OP-B exerted potent antiproliferative activity on HeLa cells, the cell growth inhibition effect of OP-B was not due to apoptosis and OP-B could induce autophagy of HeLa cells. OP-B also induced the protein expression up-regulation of Beclin-1 and promoted LC3 I transformation LC3 II, which were representative proteins of autophagy. Furthermore, 3-MA, an inhibitor of autophagy, not only inhibited OP-B-mediated autophagy but also almost completely reversed the antiproliferative effect of OP-B, suggesting that the growth inhibition effect of OP-B was autophagy dependent. Western blotting demonstrated that OP-B inhibited the phosphorylation of Akt and its' downstream vital protein, such as mTOR and p70S6K. In addition, OP-B also induced the protein expression up-regulation of PTEN, which is a negative regulation protein for Akt/mTOR signaling pathway. However, OP-B did not affect the protein expression of total Akt. Collectively, the antitumor effects of OP-B were autophagy-dependent via repression Akt/mTOR signaling pathway. Therefore, OP-B is a prospective inhibitor of Akt/mTOR and may be used as an alternative compound to treat cervical carcinoma. SN - 0513-4870 UR - https://www.unboundmedicine.com/medline/citation/23984518/[Molecular_mechanism_of_ophiopogonin_B_induced_cellular_autophagy_of_human_cervical_cancer_HeLa_cells]_ L2 - http://www.diseaseinfosearch.org/result/7949 DB - PRIME DP - Unbound Medicine ER -