Involvement of p38 mitogen‐activated protein kinase in acquired gemcitabine‐resistant human urothelial carcinoma sublines

Kao, Yu–Ting; Hsu, Wei-Chi; Hu, Huei-Ting; Hsu, Shih-Hsien; Lin, Chang-Shen; Chiu, Chien‐Chih; Lu, Chi‐Yu; Hour, Tzyh‐Chyuan; Pu, Yeong-Shiau; Huang, A-Mei

doi:10.1016/j.kjms.2014.03.004

Cited by 13 publications

(9 citation statements)

References 34 publications

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“…Resistance to chemotherapeutic drugs is one of the major challenges in the treatment of cancer. Inhibition of p38 significantly increased Gemcitabine sensitivity in bladder cancer cells [33]. Fang, Y et al reported that JNK inhibitor SP600125 suppressed anchorage-independent growth of T24T bladder cancer cells [34].…”

Section: Discussionmentioning

confidence: 99%

Cigarette smoke induced urocystic epithelial mesenchymal transition via MAPK pathways

Geng

Liu

et al. 2017

Oncotarget

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Cigarette smoke has been shown to be a major risk factor for bladder cancer. Epithelial-mesenchymal transition (EMT) is a crucial process in cancer development. The role of MAPK pathways in regulating cigarette smoke-triggered urocystic EMT remains to be elucidated. Human normal urothelial cells and BALB/c mice were used as in vitro and in vivo cigarette smoke exposure models. Exposure of human normal urothelial cells to cigarette smoke induced morphological change, enhanced migratory and invasive capacities, reduced epithelial marker expression and increased mesenchymal marker expression, along with the activation of MAPK pathways. Moreover, we revealed that ERK1/2 and p38 inhibitors, but rather JNK inhibitor, effectively attenuated cigarette smoke-induced urocystic EMT. Importantly, the regulatory function of ERK1/2 and p38 pathways in cigarette smoke-triggered urocystic EMT was further confirmed in mice exposed to CS for 12 weeks. These findings could provide new insight into the molecular mechanisms of cigarette smoke-associated bladder cancer development as well as its potential intervention.

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Section: Discussionmentioning

confidence: 99%

Cigarette smoke induced urocystic epithelial mesenchymal transition via MAPK pathways

Geng

Liu

et al. 2017

Oncotarget

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“…For example, suppression of the MEK-ERK signaling pathway by PD98059 increased rather than decreased cisplatin resistance (28). In addition, inhibition of p38 MAPK significantly reduced gemcitabine sensitivity in NTUB1 cells, and Calebin-A enhanced the cytotoxicity of vincristine in SGC7901/vincristine cells through the inhibition of JNK (29,30). The exact effect of the modulation of MAPKs depends on the cell types and crosstalk among the various pathways.…”

Section: Discussionmentioning

confidence: 99%

Triptolide exerts pro-apoptotic and cell cycle arrest activity on drug-resistant human lung cancer A549/Taxol cells via modulation of MAPK and PI3K/Akt signaling pathways

et al. 2016

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Abstract. Multidrug resistance (MDR) is a major obstacle in the effective chemotherapeutic treatment of cancers. Triptolide (TPL) is a diterpenoid isolated from Tripterygium wilfordii Hook. f., a traditional Chinese medicine. It was demonstrated in our previous study that TPL exerts anti-MDR cancers on various MDR cell lines (including A549/Taxol, MCF-7/ADR and Bel7402/5-Fu). The present study was designed to investigate its anti-proliferative activity on A549/Taxol cells, and explore the underlying mechanism of action. The anti-proliferative activity of TPL on A549/Taxol cells was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Its pro-apoptosis and cell cycle arrest activities were analyzed by flow cytometry. Western blot assay was employed to investigate the levels of mitogen-activated protein kinases (MAPKs) and apoptosis-related proteins in cells. TPL efficiently suppressed the proliferation of A549/Taxol cells. Co-treatment with MAPK inhibitors in the MTT assay indicated that the extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) pathways were involved in the process. Upregulation of p-p38, p-ERK, p-GSK-3β, Bax and cleaved caspases-3 and -9, and downregulation of p-JNK, p-Akt and Bcl-2 were observed upon treatment with TPL in the A549/Taxol cells. The results from flow cytometry assay revealed that TPL induced apoptosis and S-phase arrest in A549/Taxol cells. This occurred as a result of the upregulation of p-ERK and p-GSK-3β, and the downregulation of p-JNK and p-Akt, and was responsible for the subsequent anti-proliferative activity.

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“…P-38 has an important function in cell-cell signaling against stress and is responsive to stress stimuli, such as cytokines, ultraviolet irradiation, heat shock, and osmotic shock. It is also involved in cell differentiation, apoptosis, and autophagy [36,37]. Similarly, NF-kB plays a very important role in several cellular functions.…”

Section: Resultsmentioning

confidence: 99%

Elucidation the Toxicity Mechanism of Zinc Oxide Nanoparticle Using Molecular Docking Approach With Proteins

Singh

Dhasmana

Rahman

2018

Asian J Pharm Clin Res

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Objective: At present, toxicological tests are resource-intensive, time-consuming and require a large pool of animal models for toxicity assessment. To speed up the toxicity evaluation and to reduce animal suffering during toxicity assessment, the use of alternative methods including computational models is in high demand. The computational toxicity prediction methods are very helpful for the regulatory bodies to quickly assess the health impact of nanomaterial materials. In the present work, we have examined the mechanism of zinc oxide nanoparticle (ZnO-NP)-proteins interaction and their effect of surface chemistries of ZnO-NP on the bioactive conformation of chemokines and other cytological proteins using in silico molecular docking approaches.Methods: Molecular docking study was conducted using AutoDock 4.0 version and the visualization result using Discover Studio 4.0. Results:In the present study, we observed that ZnO-NP has high binding affinity with the mitogen-activated protein kinases (P-38), nuclear factor kappa-light-chain-enhancer of activated B cell (NF-kB) proteins, and matrix metallopeptidase-9 with docking energies −8.81, −7.64, and −7.27 Kcal/Mol, respectively, involving with hydrogen, metal acceptor, and electrostatic interaction. The top interacting amino acid residues with ZnO-NP are GLY, PHE, ARG, ASP, GLN, and ASN. Conclusion:Thus, based on the molecular docking studies, we determine that the ZnO-NP is strongly interacting with the chemokines and other cytological proteins thus responsible for blocking of the activation stimuli for these proteins to initiate the biological signals for the proper functioning. We have also extracted the information of interaction pattern of ZnO-NP with the surface-enriched amino acid residues of chemokine and cytological proteins using molecular docking approach.

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Involvement of p38 mitogen‐activated protein kinase in acquired gemcitabine‐resistant human urothelial carcinoma sublines

Cited by 13 publications

References 34 publications

Cigarette smoke induced urocystic epithelial mesenchymal transition via MAPK pathways

Cigarette smoke induced urocystic epithelial mesenchymal transition via MAPK pathways

Triptolide exerts pro-apoptotic and cell cycle arrest activity on drug-resistant human lung cancer A549/Taxol cells via modulation of MAPK and PI3K/Akt signaling pathways

Elucidation the Toxicity Mechanism of Zinc Oxide Nanoparticle Using Molecular Docking Approach With Proteins

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