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Chemotherapy induces cell plasticity;controlling plasticity increases therapeutic response

Signal Transduction and Targeted Therapy 2023年第8期8卷 3563-3566页

作者： Francisco J.Iborra Cristina Martí Virtu Calabuig-Navarro Petros Papadopoulos Salvador Meseguer Pedro M.Iborra Francisco García Antonio Martínez-Lorente Fernando Almazán Juana Calabuig Centro de Investigación Príncipe Felípe(Associated Unit to Instituto de biomedicína de Valencia) ValenciaSpain Pathology and Molecular Therapy Department Instituto de Biomedicína de Valencia(IBV)CSICValenciaSpain Molecular and Cellular Biology Department Centro Nacional de Biotecnología(CNB)CSICMadridSpain Hematology Department Hospital Clínico San CarlosMadridSpain Medical Systems Biology Faculty of MedicineUniversity of HelsinkiHelsinkiFinland ic biomed AlicanteSpain VinalopóHospitals Elcheand Biotechnology DepartmentUniversidad de AlicanteAlicanteSpain

Dear Editor,One of the most serious issues in modern oncology is the ineffectiveness of treatments in destroying tumours,which leads to tumour recurrence and,ultimately,patient death.This phenomenon is caused by conventional therapies’fractional killing of tumour cells,which can also cause resistant cells to spread.1 We analysed chemotherapy-resistant cells and discovered that they are smaller than untreated cells(Fig.1a).The fact that this phenomenon occurs in all tested cell types(Hela,A549,Huh7,and MCF7)and regardless of the chemotherapy regimen(TRAIL,Camptothecin,Doxorubicin)suggests that it is a widespread phenomenon(Fig.1a,Supplementary Fig.S1).

关键词： chemotherapy tumour plasticity

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A Thiazole Analogue Exhibits an Anti-Proliferative Effect in Different Human Carcinoma Cell Lines and Its Mechanism Based on Molecular Modeling

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Advances in Biological Chemistry 2017年第1期7卷 76-87页

作者： Hatem K. Amin Amr M. El-Araby Sameh Eid Tamer Nasr Samir Bondock Ola Leheta Moustafa E. Dawoud Department of Biochemistry and Molecular Biology Faculty of Pharmacy Helwan University Cairo Egypt Faculty of Pharmacy Ain Shams University Cairo Egypt biomed X Innovation Center Heidelberg Germany Department of Pharmaceutical Chemistry Faculty of Pharmacy Helwan University Cairo Egypt Department of Chemistry Faculty of Science Mansoura University Mansoura Egypt Department of Clinical Pathology College of Medicine Suez Canal University Ismailia Egypt Department of Organic Pharmaceutical Chemistry Faculty of Pharmacy Helwan University Cairo Egypt

Purpose: Aim of this study is to assess the anti-proliferative effect of the thiazole analogue (5-acetyl-4-methyl-2-(3-pyridyl) thiazole) with different human carcinoma cell lines and to postulate its possible mechanism of action using molecular modeling. Methods: Three different human carcinoma cell lines were used namely hepatocyte carcinoma (HEPG2), breast adenocarcinoma (MCF7) and colon cancer (HCT116). Molecular docking simulations for tested thiazole analogue and its virtual analogues against the cytochrome P-450 2A6 enzyme and mutated SOD were performed. Results: Cell lines cytotoxicity revealed that the tested thiazole analogue exerts a significant anti-proliferative activity in all the used human carcinoma cell lines with a pronounced anti-proliferative effect in liver carcinoma cell line HEPG2 (ic50 = 23.8 μg/ml) whereas the anti-proliferative effect in colon carcinoma and breast cancer cell lines was poor with ic50 = 50 μg/ml and ic50 > 50 μg/ml respectively. The postulated mechanism of action revealed the high affinity to inhibit SOD and CYP2A6 enzymes in the liver. Conclusion: The thiazole analogue (5-acetyl-4-methyl-2-(3-pyridyl)thiazole) is a potential liver specific anticancer agent capable of interfering with both apoptotic signaling pathway and the free radical processing in liver which leads to more studies on liver cancer from different perspective rather than the apoptotic signaling pathway.

关键词： Thiazole Liver Cancer Hepatocyte Carcinoma Breast Adenocarcinoma Colon Cancer Molecular Docking Superoxide Dismutase CYP2A6

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