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Mechanisms and Effects Of Downregulation Of Lactotransferrin (LTF) In Prostate Cancer
Syed Shaheduzzaman
CPDR, Rockville, MD
Introduction: Recent reports underscore the need for better prostate cancer (CaP)-specific biomarkers and therapeutic targets. This study evaluates Lactotransferrin (LTF) as one of the most common expression alterations in prostate tumor cells. LTF is an iron-binding glycoprotein found in secretions from organs including the prostate. We propose to evaluate the mechanism and effect of LTF down regulation in CaP.
Methods: RNA extracted from laser capture microdissected (LCM) matched benign and tumor cells were analyzed by GeneChip® U133a. LTF expression and copy number was analyzed in CaP specimens using QRT-PCR. LTF protein level was evaluated in CaP tissue by immunohistochemistry (IHC). Serum LTF levels were measured in 34 CaP patients and 35 healthy male controls using ELISA. Chemopreventive effect of LTF was evaluated in LNCaP cells by cell proliferation assay. LTF methylation was analyzed in LNCaP cells using EpiTYPER, MALDI-TOF MS (SEQUENOM).
Results: GeneChip® analysis revealed significant downregulation of LTF in CaP (p<10-6). Lower LTF copy number was observed in 74% of CaP specimens (n=100). Significantly decreased LTF protein level was observed in tumor glands in 30 of 30 CaP tissue specimens and also in serum of 34 CaP patients (p<0.0001). LNCaP cell proliferation was significantly inhibited by 10μmol/L lactoferrin (p < 0.01) indicating potential therapeutic implication in CaP. One target region of LTF showed 74 to 97% LTF methylation alterations in 80% of the analyzed CpG sites.
Conclusion: Our results identify
LTF down regulation as a potential biomarker for CaP and may also play a role in prostate carcinogenesis.
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