2019
DOI: 10.1186/s13046-019-1161-8
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Inhibition of ATM reverses EMT and decreases metastatic potential of cisplatin-resistant lung cancer cells through JAK/STAT3/PD-L1 pathway

Abstract: Background The cisplatin-resistance is still a main course for chemotherapy failure of lung cancer patients. Cisplatin-resistant cancer cells own higher malignance and exhibited increased metastatic ability, but the mechanism is not clear. In this study, we investigated the effects of Ataxia Telangiectasia Mutated (ATM) on lung cancer metastasis. Materials and methods Cisplatin-resistant A549CisR and H157CisR cell line were generated by long-term treating parental A549 … Show more

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Cited by 145 publications
(114 citation statements)
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“…385,386 In addition to being involved in DOX resistance, the contributions to chemotherapy resistance made by reciprocal and complementary interactions between EMT and PD-L1 have been further validated in cisplatin (DDP) resistance of NSCLC cells. A possible mechanism in this study was attributed to the activation of the JAK/STAT3 pathway in an ataxia telangiectasia mutated-dependent manner, 388 largely in agreement with the previous reports. 368,389 Collectively, these observations provide strong evidence that the tight interactions between EMT programming and PD-L1 expression contribute critically to the development of resistance to either chemotherapeutics or targeted drugs, with or without the involvement of EMT/PD-L1-related immune escape.…”
Section: Epithelial-mesenchymal Transition (Emt)supporting
confidence: 93%
“…385,386 In addition to being involved in DOX resistance, the contributions to chemotherapy resistance made by reciprocal and complementary interactions between EMT and PD-L1 have been further validated in cisplatin (DDP) resistance of NSCLC cells. A possible mechanism in this study was attributed to the activation of the JAK/STAT3 pathway in an ataxia telangiectasia mutated-dependent manner, 388 largely in agreement with the previous reports. 368,389 Collectively, these observations provide strong evidence that the tight interactions between EMT programming and PD-L1 expression contribute critically to the development of resistance to either chemotherapeutics or targeted drugs, with or without the involvement of EMT/PD-L1-related immune escape.…”
Section: Epithelial-mesenchymal Transition (Emt)supporting
confidence: 93%
“…EMT has been revealed to be of vital importance in the early events of cancer cell metastatic dissemination by endowing cells with a more motile, invasive potential (22). E-cadherin, vimentin and N-cadherin are the recognized molecular markers participating in EMT (23). During migration and invasion, the expression of E-cadherin is reduced while that of vimentin and N-cadherin is increased (24).…”
Section: Discussionmentioning
confidence: 99%
“…Furthermore, CD163 is considered the most speci c marker of TAMS, involved in the occurrence, development, migration, angiogenesis, EMT, etc., of GBM [42,43]. PD-L1 is the focus of current immunotherapy research, the study found that its expression is closely related to EMT [44,45], and EMT is the focus of current cancer resistance research [46,47]. But no research has been done to explore the causes of individualization of patient therapy through their relationship.…”
Section: Discussionmentioning
confidence: 99%