Cell apoptosis, autophagy and necroptosis in osteosarcoma treatment

Jing Li, Zuozhang Yang _, Yi Li, Junfeng Xia, Dongqi Li, Huiling Li, Mingyan Ren, Yedan Liao, Shunling Yu, Yanjin Chen, Yihao Yang and Ya Zhang

PDF  |  HTML  |  How to cite  |  Order a Reprint

Oncotarget. 2016; 7:44763-44778. https://doi.org/10.18632/oncotarget.8206

Metrics: PDF 2780 views  |   HTML 3862 views  |   ?  


Jing Li1,2,*, Zuozhang Yang1,*, Yi Li3,*, Junfeng Xia1,*, Dongqi Li1, Huiling Li1, Mingyan Ren1, Yedan Liao1, Shunling Yu1, Yanjin Chen1, Yihao Yang1 and Ya Zhang1

1 Bone and Soft Tissue Tumors Research Center of Yunnan Province, Department of Orthopaedics, the Third Affiliated Hospital of Kunming Medical University (Tumor Hospital of Yunnan Province), Kunming, Yunnan, China

2 State Key Laboratory of Protein and Plant Gene Research, College of Life Sciences, Peking University, Beijing, China

3 Department of Oncology, Kunming General Hospital of Chengdu Military Command, Kunming, Yunnan, China

* These authors have contributed equally to this work

Correspondence to:

Zuozhang Yang, email:

Keywords: apoptosis, autophagy, necroptosis, chemotherapy resistance, osteosarcoma

Received: January 02, 2016 Accepted: March 07, 2016 Published: March 19, 2016


Osteosarcoma is the most common primary bone tumor in children and adolescents. Although combined therapy including surgery and multi-agent chemotherapy have resulted in great improvements in the overall survival of patients, chemoresistance remains an obstacle for the treatment of osteosarcoma. Molecular targets or effective agents that are actively involved in cell death including apoptosis, autophagy and necroptosis have been studied. We summarized how these agents (novel compounds, miRNAs, or proteins) regulate apoptotic, autophagic and necroptotic pathways; and discussed the current knowledge on the role of these new agents in chemotherapy resistance in osteosarcoma.

Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.
PII: 8206