NDLI: KRAS NF-κB is involved in the development of zinc resistance and reduced curability in prostate cancer

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Zinc ions modulate protein tyrosine phosphatase 1B activity

KRAS NF-κB is involved in the development of zinc resistance and reduced curability in prostate cancer

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Metallomics Vol - 6 Issue - 6

Metallomics Vol - 6 Issue - 5

Metallomics Vol - 6 Issue - 4

Metallomics Vol - 6 Issue - 3

Metallomics Vol - 6 Issue - 2

KRAS NF-κB is involved in the development of zinc resistance and reduced curability in prostate cancer

Content Provider	Royal Society of Chemistry (RSC)
Author	Holubova, Monika Raudenska, Martina Adam, Vojtech Masarik, Michal Gumulec, Jaromir Kizek, Rene Sztalmachova, Marketa Axmanova, Martina Babula, Petr
Copyright Year	2014
Abstract	Zinc(II) ions are important components of many proteins and are involved in numerous cellular processes such as apoptosis or drug resistance. Prostate cancer has a unique relationship with zinc(II) ions. However, the relationship was examined only in short-term zinc(II) treatments. Therefore, the aim of this study was to create zinc-resistant prostatic cell lines at various stages of the disease (22Rv1 and PC-3) and a normal prostate epithelium (PNT1A) using a long-term zinc exposure. Consequently, the expression profile of the following genes was analyzed: BAX, Bcl-2, Beclin-1, CFLAR, HIF1α, KRAS, mTOR, MT1A, MT2A, NF-κB1, p53, survivin, ZIP1, ZnT-1. The resistance was verified using the MTT test; on average a 1.35-fold lower zinc(II) toxicity (higher IC50) was determined in zinc(II)-resistant cells. The associated resistance to cisplatin was also determined; IC50 for cisplatin was 1.52-fold higher. With regard to the gene expression profiles, our results indicate that differential mechanisms participate in the short-term zinc toxicity regulation and long-term resistance; the short-term treatment was associated with MT2A (p < 0.001), ZnT-1 (p < 0.001), and MT1A (p < 0.03) and the long-term resistance was associated particularly with NF-κB1 (p < 0.001), CFLAR (p < 0.001), KRAS (p < 0.001), p53 (p < 0.002), survivin (p = 0.02), ZIP1 (p = 0.002), BAX (p = 0.005), and HIF1α (p = 0.05). Therefore, the KRAS-PI3K-NF-κB pathway is expected to play a crucial role in the regulation of zinc resistance. In summary, compared to previous studies, identical mechanisms of resistance were demonstrated on multiple cell lines, both non-tumor and tumorous, derived both from primary and advanced secondary sites.
Starting Page	1240
Ending Page	1253
Page Count	14
File Format	HTM / HTML PDF
ISSN	17565901
Volume Number	6
Issue Number	7
Journal	Metallomics
DOI	10.1039/c4mt00065j
Language	English
Publisher	Royal Society of Chemistry
Access Restriction	Open
Subject Keyword	Bcl-2 PC3 BECN1 Mechanistic target of rapamycin CFLAR Epithelium Zinc toxicity Zinc Cisplatin P53 Gene IC50 KRAS Prostate cancer Prostate SLC39A1 Apoptosis
Content Type	Text
Resource Type	Article
Subject	Chemistry Medicine Metals and Alloys Biochemistry Biomaterials Biophysics

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KRAS NF-κB is involved in the development of zinc resistance and reduced curability in prostate cancer

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KRAS NF-κB is involved in the development of zinc resistance and reduced curability in prostate cancer