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. 2019 Oct 18;55(6):1213–1222. doi: 10.3892/ijo.2019.4902

Figure 2.

Figure 2

Autophagy regulates OS chemoresistance, metastasis and tumor immunity. HMGB1, GFRA1, HMGN5, IGF2, DNA-PKcs, NDRG1 and HSP90AA1 induced by chemotherapeutic drugs activate cytoprotective autophagy and contribute to chemoresistance in OS. In addition, miRNAs increase OS chemosensitivity by either inhibiting cytoprotective autophagy or inducing autophagic cell death. NVP-BEZ235 (a PI3K/mTOR inhibitor), TSSC3 and certain Chinese herbs enhance chemosensitivity in OS by increasing apoptosis which is dependent of autophagic cell death. COPS3 knockdown and metformin reduce autophagy-mediated metastasis in OS. Polymeric chloroquine decreased CXCR4-mediated OS metastasis, and this effect was autophagy-independent. PD-L1 suppression by 3-MA and PD-L2 knockdown enhanced immunological response and inhibited OS metastasis. HMGB1, High mobility group box 1; GFRA1, GDNF receptor α1; HMGN5, high-mobility group nucleosome-binding domain 5; IGF2, insulin growth factor 2; DNA-PKcs, DNA-dependent protein kinase catalytic subunit; miRNA, microRNA; NDRG1, N-myc downstream-regulated gene 1; HSP90AA1, heat shock protein 90AA1; OS, osteosarcoma; TSSC3, tumor-suppressing STF cDNA 3; COPS3, COP9 signalosome subunit 3; CXCR4, chemokine receptor 4; PD-L, programmed death ligand; 3-MA, 3-methyladenine.