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Inhibiting ROS-TFEB-Dependent Autophagy Enhances Salidroside-Induced Apoptosis in Human Chondrosarcoma Cells.
Cell Physiol Biochem. 2017; 43(4):1487-1502.CP

Abstract

BACKGROUND/AIMS

Autophagy modulation has been considered a potential therapeutic strategy for human chondrosarcoma, and a previous study indicated that salidroside exhibits significant anti-carcinogenic activity. However, the ability of salidroside to induce autophagy and its role in human chondrosarcoma cell death remains unclear.

METHODS

We exposed SW1353 cells to different concentrations of salidroside (0.5, 1 and 2 mM) for 24 h. RT-PCR, Western-blotting, Immunocytofluorescence, and Luciferase Reporter Assays were used to evaluate whether salidroside activated the TFEB-dependent autophagy.

RESULTS

We show that salidroside induced significant apoptosis in the human chondrosarcoma cell line SW1353. In addition, we demonstrate that salidroside-induced an autophagic response in SW1353 cells, as evidenced by the upregulation of LC3-II and downregulation of P62. Moreover, pharmacological or genetic blocking of autophagy enhanced salidroside -induced apoptosis, indicating the cytoprotective role of autophagy in salidroside-treated SW1353 cells. Salidroside also induced TFEB (Ser142) dephosphorylation, subsequently to activated TFEB nuclear translocation and increase of TFEB reporter activity, which contributed to lysosomal biogenesis and the expression of autophagy-related genes. Importantly, we found that salidroside triggered the generation of ROS in SW1353 cells. Furthermore, NAC, a ROS scavenger, abrogated the effects of salidroside on TFEB-dependent autophagy.

CONCLUSIONS

These data demonstrate that salidroside increased TFEB-dependent autophagy by activating ROS signaling pathways in human chondrosarcoma cells. These data also suggest that blocking ROS-TFEB-dependent autophagy to enhance the activity of salidroside warrants further attention in treatment of human chondrosarcoma cells.

Authors+Show Affiliations

Department of Orthopedics Surgery, Second Xiangya Hospital of Central South University, Changsha, China. Department of Orthopedics Surgery, Central Hospital of Zhuzhou City and Affiliated Zhuzhou Hospital of Xiangya Medical College of Central South University, Zhuzhou, China.Department of Orthopedics Surgery, Second Xiangya Hospital of Central South University, Changsha, China.Department of Orthopedics Surgery, Central Hospital of Zhuzhou City and Affiliated Zhuzhou Hospital of Xiangya Medical College of Central South University, Zhuzhou, China.Department of Orthopedics Surgery, Second Xiangya Hospital of Central South University, Changsha, China.Department of Infectious Diseases, Central Hospital of Zhuzhou City and Affiliated Zhuzhou Hospital of Xiangya Medical College of Central South University, Zhuzhou, China.Department of Orthopedics Surgery, Central Hospital of Zhuzhou City and Affiliated Zhuzhou Hospital of Xiangya Medical College of Central South University, Zhuzhou, China.Department of Orthopedics Surgery, Central Hospital of Zhuzhou City and Affiliated Zhuzhou Hospital of Xiangya Medical College of Central South University, Zhuzhou, China.Surgery Department of Galactophore, Central Hospital of Zhuzhou City and Affiliated Zhuzhou Hospital of Xiangya Medical College of Central South University, Zhuzhou, China.Department of Intergrated traditional Chinese medicine and western medicine, Central Hospital of Zhuzhou City and Affiliated Zhuzhou Hospital of Xiangya Medical College of Central South University, Zhuzhou, China.Department of Orthopedics Surgery, Central Hospital of Zhuzhou City and Affiliated Zhuzhou Hospital of Xiangya Medical College of Central South University, Zhuzhou, China.Department of Orthopedics Surgery, Central Hospital of Zhuzhou City and Affiliated Zhuzhou Hospital of Xiangya Medical College of Central South University, Zhuzhou, China.Department of Orthopedics Surgery, Central Hospital of Zhuzhou City and Affiliated Zhuzhou Hospital of Xiangya Medical College of Central South University, Zhuzhou, China.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

29035891

Citation

Zeng, Wei, et al. "Inhibiting ROS-TFEB-Dependent Autophagy Enhances Salidroside-Induced Apoptosis in Human Chondrosarcoma Cells." Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology, vol. 43, no. 4, 2017, pp. 1487-1502.
Zeng W, Xiao T, Cai A, et al. Inhibiting ROS-TFEB-Dependent Autophagy Enhances Salidroside-Induced Apoptosis in Human Chondrosarcoma Cells. Cell Physiol Biochem. 2017;43(4):1487-1502.
Zeng, W., Xiao, T., Cai, A., Cai, W., Liu, H., Liu, J., Li, J., Tan, M., Xie, L., Liu, Y., Yang, X., & Long, Y. (2017). Inhibiting ROS-TFEB-Dependent Autophagy Enhances Salidroside-Induced Apoptosis in Human Chondrosarcoma Cells. Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology, 43(4), 1487-1502. https://doi.org/10.1159/000481971
Zeng W, et al. Inhibiting ROS-TFEB-Dependent Autophagy Enhances Salidroside-Induced Apoptosis in Human Chondrosarcoma Cells. Cell Physiol Biochem. 2017;43(4):1487-1502. PubMed PMID: 29035891.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Inhibiting ROS-TFEB-Dependent Autophagy Enhances Salidroside-Induced Apoptosis in Human Chondrosarcoma Cells. AU - Zeng,Wei, AU - Xiao,Tao, AU - Cai,Anlie, AU - Cai,Weiliang, AU - Liu,Huanhuan, AU - Liu,Jingling, AU - Li,Jie, AU - Tan,Miduo, AU - Xie,Li, AU - Liu,Ying, AU - Yang,Xiangcheng, AU - Long,Yi, Y1 - 2017/10/16/ PY - 2017/07/14/received PY - 2017/09/14/accepted PY - 2017/10/17/pubmed PY - 2017/12/19/medline PY - 2017/10/17/entrez KW - Apoptosis KW - Autophagy KW - Chondrosarcoma KW - Reactive Oxygen Species KW - Salidroside KW - TFEB SP - 1487 EP - 1502 JF - Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology JO - Cell. Physiol. Biochem. VL - 43 IS - 4 N2 - BACKGROUND/AIMS: Autophagy modulation has been considered a potential therapeutic strategy for human chondrosarcoma, and a previous study indicated that salidroside exhibits significant anti-carcinogenic activity. However, the ability of salidroside to induce autophagy and its role in human chondrosarcoma cell death remains unclear. METHODS: We exposed SW1353 cells to different concentrations of salidroside (0.5, 1 and 2 mM) for 24 h. RT-PCR, Western-blotting, Immunocytofluorescence, and Luciferase Reporter Assays were used to evaluate whether salidroside activated the TFEB-dependent autophagy. RESULTS: We show that salidroside induced significant apoptosis in the human chondrosarcoma cell line SW1353. In addition, we demonstrate that salidroside-induced an autophagic response in SW1353 cells, as evidenced by the upregulation of LC3-II and downregulation of P62. Moreover, pharmacological or genetic blocking of autophagy enhanced salidroside -induced apoptosis, indicating the cytoprotective role of autophagy in salidroside-treated SW1353 cells. Salidroside also induced TFEB (Ser142) dephosphorylation, subsequently to activated TFEB nuclear translocation and increase of TFEB reporter activity, which contributed to lysosomal biogenesis and the expression of autophagy-related genes. Importantly, we found that salidroside triggered the generation of ROS in SW1353 cells. Furthermore, NAC, a ROS scavenger, abrogated the effects of salidroside on TFEB-dependent autophagy. CONCLUSIONS: These data demonstrate that salidroside increased TFEB-dependent autophagy by activating ROS signaling pathways in human chondrosarcoma cells. These data also suggest that blocking ROS-TFEB-dependent autophagy to enhance the activity of salidroside warrants further attention in treatment of human chondrosarcoma cells. SN - 1421-9778 UR - https://www.unboundmedicine.com/medline/citation/29035891/Inhibiting_ROS_TFEB_Dependent_Autophagy_Enhances_Salidroside_Induced_Apoptosis_in_Human_Chondrosarcoma_Cells_ L2 - https://www.karger.com?DOI=10.1159/000481971 DB - PRIME DP - Unbound Medicine ER -