The role of PTP1B in the drug induced ER stress

我们认为PTP1B是治疗骨肉瘤的潜在靶点。骨肉瘤细胞系PTP1B基因被敲除后，显示DOX诱导的内质网应激增加。为了评估增加的内质网应激在细胞中的功能，我们评估了自噬的标志物LC3的水平。因此，PTP1B基因敲除后Lc3降低，提示PTP1B基因敲除可能通过增加内质网应激增加化疗的敏感性。

We showed PTP1B is a potential target of the therapy of osteosarcoma. Knock down of PTP1B in the cell line of osteosarcoma showed increased ER stress induced by DOX. To assess the function of increased ER stress in the cells, we assessed the level of LC3 which is a marker of autophagy. as a result, LC3 decreased after PTP1B knock down which suggests that PTP1B knock down potentially increase the susceptivity to chemotherapy through increased ER stress.