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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Bhattacharya, Surela Das, Amlan Datta, Satabdi Ganguli, Arnab Chakrabarti, Gopal |
| Description | Country affiliation: India Author Affiliation: Bhattacharya S ( Department of Biotechnology and Dr. B.C. Guha Centre for Genetic Engineering and Biotechnology, University of Calcutta, 35 Ballygunge Circular Road, Kolkata, WB, 700 019, India.); Das A ( Department of Biotechnology and Dr. B.C. Guha Centre for Genetic Engineering and Biotechnology, University of Calcutta, 35 Ballygunge Circular Road, Kolkata, WB, 700 019, India.); Datta S ( Department of Biotechnology and Dr. B.C. Guha Centre for Genetic Engineering and Biotechnology, University of Calcutta, 35 Ballygunge Circular Road, Kolkata, WB, 700 019, India.); Ganguli A ( Department of Biotechnology and Dr. B.C. Guha Centre for Genetic Engineering and Biotechnology, University of Calcutta, 35 Ballygunge Circular Road, Kolkata, WB, 700 019, India.); Chakrabarti G ( Department of Biotechnology and Dr. B.C. Guha Centre for Genetic Engineering and Biotechnology, University of Calcutta, 35 Ballygunge Circular Road, Kolkata, WB, 700 019, India. gcbcg@caluniv.ac.in.) |
| Abstract | Colchicine is a well-known and potent microtubule targeting agent, but the therapeutic value of colchicine against cancer is limited by its toxicity against normal cells. But, there is no report of its cytotoxic potential against lung cancer cell, at clinically permissible or lower concentrations, minimally toxic to non-cancerous cells. Hence, in the present study, we investigated the possible mechanism by which the efficacy of colchicine against lung cancer cells at less toxic dose could be enhanced. Colchicine at clinically admissible concentration of 2.5 nM had no cytotoxic effect and caused no G2/M arrest in A549 cells. However, at this concentration, colchicine strongly hindered the reformation of cold depolymerised interphase and spindle microtubule. Colchicine induced senescence and reactive oxygen species mediated autophagy in A549 cells at this concentration. Autophagy inhibitor 3-methyladenine (3-MA) sensitised the cytotoxicity of colchicine in A549 cells by switching senescence to apoptotic death, and this combination had reduced cytotoxicity to normal lung fibroblast cells (WI38). Together, these findings indicated the possible use of colchicine at clinically relevant dose along with autophagy inhibitor in cancer therapy. |
| File Format | HTM / HTML |
| ISSN | 10104283 |
| Issue Number | 8 |
| Journal | Tumor Biology |
| Volume Number | 37 |
| e-ISSN | 14230380 |
| Language | English |
| Publisher | Springer |
| Publisher Date | 2016-08-01 |
| Publisher Place | Netherlands |
| Access Restriction | Subscribed |
| Content Type | Text |
| Resource Type | Article |
| Subject | Medicine Cancer Research |
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