Downregulation of DOCK1 sensitizes bladder cancer cells to cisplatin through preventing epithelial&amp;ndash;mesenchymal transition

Chen, Dajin; Chen, Wei; Jiang, Hong; Yang, Hao; Wang, Yucheng; Chen, Jianghua

doi:10.2147/dddt.s101998

Cited by 14 publications

(11 citation statements)

References 30 publications

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“…18,47 Cisplatin treatment inhibited the expression of E-cadherin and promoted the expression of vimentin in bladder cancer cell, and the cisplatin sensitivity was remarkably enhanced after EMT blockage. 48 It was also showed that EMT was necessary for acquired resistance to cisplatin and increased the metastatic potential of NPC cells. 49 Corresponded with these reports, our results showed that DDP-resistant NPC cells acquired EMT features and enhanced migration and invasion potential.…”

Section: Discussionmentioning

confidence: 99%

Hippo pathway contributes to cisplatin resistant-induced EMT in nasopharyngeal carcinoma cells

Zhang

et al. 2017

Cell Cycle

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Nasopharyngeal carcinoma (NPC) is a kind of head-neck malignant tumor derived from the nasopharyngeal epithelium and is mainly prevalent in Southern China and Southeast Asia countries. Cisplatin (DDP) provides the first-line therapeutic administration in NPC patients. However, chemoresistance has been a main barrier and caused bad treatment outcome in NPC therapy. To understand the molecular mechanism of acquired resistance to DDP, multiple methods were performed to examine the morphocytology and molecular changes in DDP-resistant NPC cells. We found that drug resistance cells displayed epithelial-mesenchymal transition (EMT) characteristics. DDP-resistant NPC cells exhibited enhanced migration and invasion potential. Moreover, overexpression of TAZ, one key gene in Hippo pathway, is closely associated with the DDP resistance of NPC cells and its EMT properties. Depletion of TAZ in DDP-resistant cells reversed EMT phenotypes to MET characteristics and restored chemosensitivity of DDP-resistant cells to DDP treatment. These results suggest that inactivation of TAZ could be a promising approach for the treatment of NPC patients.

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Section: Discussionmentioning

confidence: 99%

Hippo pathway contributes to cisplatin resistant-induced EMT in nasopharyngeal carcinoma cells

Zhang

et al. 2017

Cell Cycle

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“…In human colorectal cancer, DOCK1 was simulated by cortactin, which could promote cell migration and invasion 26. Downregulation of DOCK1 may prevent epithelial–mesenchymal transition in bladder cancer 16. Furthermore, in vivo researches by Tajiri, et al have demonstrated the effectiveness of targeting DOCK1 in the ras-driven cancer cell 27.…”

Section: Discussionmentioning

confidence: 99%

“…The dedicator of cytokinesis 1 (DOCK) family is a class of the atypical Rho guanine nucleotide exchange factors (GEFs) 16. As a major Rac GEF, DOCK proteins are involved in various cellular processes, such as cell adhesion, cell migration, actin cytoskeleton, and tumorigenesis 17,18.…”

Section: Introductionmentioning

confidence: 99%

<p>High expression of dedicator of cytokinesis 1 adversely influences the prognosis of acute myeloid leukemia patients undergoing allogeneic hematopoietic stem cell transplantation</p>

Zhang

Yang

et al. 2019

CMAR

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Background: Overexpression of dedicator of cytokinesis 1 ( DOCK 1) has been confirmed as an unfavorable prognostic marker in acute myeloid leukemia (AML). Purpose: This study is to explore the clinical implications of DOCK1 on AML patients underwent allogeneic hematopoietic stem cell transplantation (allo-HSCT). Patients and methods: We analyzed 71 de novo AML patients treated with allo-HSCT and divided them into two groups ( DOCK1 high vs DOCK1 low ) by the median expression level of DOCK1 . Results: High DOCK1 expression was associated with older age ( P =0.019), wild-type CEBPA ( P =0.002), IDH1/2 mutations ( P =0.010) and RUNX1 mutation ( P =0.005). Univariate analyses showed that DOCK1 high and RUNX1 mutation were associated with shorter OS ( P <0.001, P =0.024). Multivariate analysis confirmed the negative effect of high DOCK1 level on overall survival ( P =0.010). Conclusion: Our results demonstrate that in AML patients who received allo-HSCT, high DOCK1 expression might have a persistent negative prognostic impact post-transplant.

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“…39 One study demonstrated that downregulation of Dedicator of cytokinesis 1 (DOCK1) could increase the chemosensitivity in bladder cancer cells via preventing DDPinduced EMT. 40 DDP-resistant lung adenocarcinoma cells acquired mesenchymal features and were along with low expression of miR-206 and high migration and invasion abilities. 41 In NPC cells, Zhang and the colleagues described that the DDP-resistant cells exhibited morphological and molecular changes consistent with EMT, including the suppression of Ecadherin and b¡catenin and the increase of vimentin, fibronectin and MMP-9, Snail, Slug, Twist and ZEB1.…”

Section: Discussionmentioning

confidence: 99%

NEDD4 is involved in acquisition of epithelial-mesenchymal transition in cisplatin-resistant nasopharyngeal carcinoma cells

Feng

Yang

et al. 2017

Cell Cycle

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Nasopharyngeal carcinoma (NPC) is a highly invasive head-neck cancer derived from the nasopharyngeal epithelium, mainly prevalent in southern China and Southeast Asia. Radiotherapy and adjuvant cisplatin (DDP) chemotherapy are standard administrations applied in the treatment of NPC. However, resistance to chemotherapeutic drugs has recently become more common, resulting in worse treatment outcome for NPC therapy. To elucidate the underlying molecular basis of drug resistance to DDP in NPC cells, we examined the morphocytology, cell motility and molecular changes in DDP-resistant NPC cells with respect to epithelial-mesenchymal transition (EMT) features. We found that EMT is closely associated with DDP-induced drug resistance in NPC cells, as DDP-resistant cells displayed morphological and molecular markers changes consistent with EMT. Wound healing and Transwell Boyden chamber assays revealed an enhanced migration and invasion potential in DDP-resistant NPC cells. Mechanistically, upregulation of NEDD4 was observed to relate to EMT in DDP-resistant cells. More importantly, depletion of NEDD4 in resistant cells led to a partial reversion of EMT phenotypes to MET characteristics. These data suggest that NEDD4 is largely involved in EMT features and chemoresistance of NPC cancer cells. NEDD4 could be a novel therapeutic target to overcome drug resistance in successful administrations of NPC.

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Downregulation of DOCK1 sensitizes bladder cancer cells to cisplatin through preventing epithelial–mesenchymal transition

Cited by 14 publications

References 30 publications

Hippo pathway contributes to cisplatin resistant-induced EMT in nasopharyngeal carcinoma cells

Hippo pathway contributes to cisplatin resistant-induced EMT in nasopharyngeal carcinoma cells

<p>High expression of dedicator of cytokinesis 1 adversely influences the prognosis of acute myeloid leukemia patients undergoing allogeneic hematopoietic stem cell transplantation</p>

NEDD4 is involved in acquisition of epithelial-mesenchymal transition in cisplatin-resistant nasopharyngeal carcinoma cells

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