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https://www.um.edu.mt/library/oar/handle/123456789/99215
Title: | Resistance to gemcitabine in the pancreatic cancer cell line KLM1-R reversed by metformin action |
Authors: | Baron, Byron Wang, Yufeng Maehara, Shin-Ichiro Maehara, Yoshihiko Kuramitsu, Yasuhiro Nakamura, Kazuyuki |
Keywords: | Pancreas -- Cancer Metformin Heat shock proteins Drug resistance in cancer cells Medical biochemistry |
Issue Date: | 2015 |
Publisher: | International Institute of Anticancer Research |
Citation: | Baron, B., Wang, Y., Maehara, S. I., Maehara, Y., Kuramitsu, Y., & Nakamura, K. (2015). Resistance to gemcitabine in the pancreatic cancer cell line KLM1-R reversed by metformin action. Anticancer Research, 35(4), 1941-1949. |
Abstract: | Background/Aim. The pancreatic cancer cell line KLM1 can gain chemoresistance following gemcitabine (GEM) treatment. Metformin was found to be a useful sensitsing agent towards GEM treatment following gain of chemoresistance. Materials and Methods: The proliferation of GEM-sensitive and -resistant cells was investigated over a range of metformin concentrations from 0.005 to 5 mM. The intra- and extra- cellular energetic profiles of these two cell types under metformin exposure were investigated through adenosine triphosphate (ATP) and L-lactate assays. Results: There was an unexpected decrease in intracellular L-lactate following gain of chemoresistance, despite observable medium acidification. At the biochemical level, a marked effect on phosphorylated proteins upstream of Akt, along the mTOR pathway, was observed at 6 h. These changes followed a time-dependent pattern linked closely to the changes in the energetic profile. Conclusion: Together, these results indicate that metformin indirectly blocks protein phosphorylation, including that of heat shock protein 27 (HSP27). |
URI: | https://www.um.edu.mt/library/oar/handle/123456789/99215 |
ISSN: | 0250-7005 |
Appears in Collections: | Scholarly Works - CenMMB |
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