Differential expression of metallothioneins (MTs) 1, 2, and 3 in response to zinc treatment in human prostate normal and malignant cells and tissues.

Molecular Cancer
Hua WeiP Feng

Abstract

The disturbance of zinc homeostasis featured with a significant decrease of cellular zinc level was well documented to associate with the development and progression of human prostate malignancy. We have previously reported that zinc treatment induces prostate malignant cell apoptosis through mitochondrial pathway. Metallothionein (MT) is a major receptor/donor of zinc in the cells. However, the studies on the expression of MT in association with the prostate pathological and malignant status are very limited, and the zinc regulation of MT isoform expression in prostate cells remains elusive. The goals of this study were to define the expression of endogenous MTs, the isoforms of MT 1, 2, 3 at both messenger ribonucleic acid (mRNA) and protein levels; and to investigate the zinc effect on MT expression in normal prostate, benign prostatic hyperplasia (BPH) and malignant PC-3 cells, and in relevant human tissues. Cellular MT proteins were detected by immunohistochemistry, fluorescence staining and Western blot analysis; reverse transcription polymerase chain reaction (RT-PCR) was used to determine the MT isoform-specific mRNAs. Our results demonstrated a significant suppression of endogenous levels of MT1/2 in malignant PC-3 cel...Continue Reading

References

Jul 15, 1992·Proceedings of the National Academy of Sciences of the United States of America·R D PalmiterD M Durnam
Sep 14, 1995·Biochemical and Biophysical Research Communications·M C AmoureuxP J Pauwels
Jun 4, 1999·Toxicology Letters·S H GarrettD A Sens
May 10, 2000·The Journal of Nutrition·R S MacDonald
May 23, 2002·Cellular and Molecular Life Sciences : CMLS·P CoyleA M Rofe
Sep 5, 2002·The Prostate·Pei FengLeslie C Costello
Nov 12, 2002·Environmental Health Perspectives·Samson T JacobKalpana Ghoshal
Dec 11, 2002·European Journal of Biochemistry·Masuo KondohMasao Sato
May 7, 2004·Toxicological Sciences : an Official Journal of the Society of Toxicology·Seema SomjiDonald A Sens
Jul 29, 2004·Histopathology·S E TheocharisG P Kouraklis
Feb 16, 2005·Apoptosis : an International Journal on Programmed Cell Death·E A Ostrakhovitch, M G Cherian
Sep 13, 2005·Molecular Cancer·Renty B FranklinLeslie C Costello
Apr 1, 2006·Journal of Clinical Pathology·S L El SharkawyM A El Shaer
Jun 6, 2006·Genes & Development·Michael T MarrRobert Tjian
Jun 24, 2006·The Journal of Biological Chemistry·Robert J CousinsLouis A Lichten
Aug 10, 2006·Proceedings of the National Academy of Sciences of the United States of America·Kevin J WrightRobert Tjian
Aug 29, 2006·Biochimie·J-P BourdineaudJ-L Moreau
Oct 5, 2006·Experimental Biology and Medicine·Michael AschnerJoao B T Rocha
Nov 1, 2006·Journal of Environmental Pathology, Toxicology and Oncology : Official Organ of the International Society for Environmental Toxicology and Cancer·Stefania FrassinettiClara Della Croce

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Citations

Jul 14, 2010·PloS One·Vojtech AdamRene Kizek
Jan 15, 2014·PloS One·Jaromir GumulecMichal Masarik
Dec 18, 2013·Proceedings of the National Academy of Sciences of the United States of America·Wen ChyanRobert J Radford
Jul 25, 2009·Biometals : an International Journal on the Role of Metal Ions in Biology, Biochemistry, and Medicine·Andrzej SapotaAnna Kilanowicz
Jul 16, 2014·Cancer Investigation·Ryan P LangeMatthias Holdhoff
Mar 12, 2015·Molecular Medicine Reports·Shinichiro Takahashi
Sep 21, 2010·Life Sciences·Akiko HondaMasahiko Satoh
Nov 17, 2009·Clinica Chimica Acta; International Journal of Clinical Chemistry·Sivanantham BanudeviJagadeesan Arunakaran
Apr 10, 2009·Molecular and Cellular Endocrinology·Zhi-Min LiuGeorge G Chen
Apr 8, 2009·Progress in Histochemistry and Cytochemistry·Mie Ø PedersenMilena Penkowa
May 29, 2014·Cell Cycle·Chandra K SinghNihal Ahmad
Dec 31, 2008·Journal of Structural Biology·Elia DiestraCristina Risco
Sep 27, 2013·Metallomics : Integrated Biometal Science·Martina RaudenskaMichal Masarik
May 18, 2012·Integrative Biology : Quantitative Biosciences From Nano to Macro·Michal MasarikRene Kizek
Aug 18, 2009·Current Opinion in Clinical Nutrition and Metabolic Care·Emily Ho, Yang Song
Dec 9, 2017·Signal Transduction and Targeted Therapy·Elizabeth BafaroRobert E Dempski
Mar 22, 2014·Biomedical Reports·Takashi OtsukaKazuyuki Hirano
Mar 1, 2019·International Journal of Molecular Sciences·Ke-Hung TsuiHorng-Heng Juang
Apr 21, 2021·Metallomics : Integrated Biometal Science·Kathrin SchillingFiona Larner

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electrophoresis
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