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Growth inhibition of thyroid follicular cell-derived cancers by the opioid growth factor (OGF) - opioid growth factor receptor (OGFr) axis
BMC Cancer, 10/21/09

McLaughlin PJ et al. – These data suggest that OGF and OGFr are present in follicular-derived thyroid cancers, and that OGF serves in a tonically active inhibitory manner to maintain homeostasis of cell proliferation. These results may provide a biotherapeutic strategy in the treatment of these cancers.

Methods

Utilizing human ATC (KAT-18), PTC (KTC-1), and FTC (WRO 82-1) cell lines, immunohistochemistry employed to ascertain presence and location of OGF and OGFr
Growth characteristics in presence of OGF or opioid antagonist naltrexone (NTX), and specificity of opioid peptides for proliferation of ATC, established in KAT-18 cells
Dependence on peptide and receptor investigated using neutralization studies with antibodies and siRNA experiments, respectively
Mechanism of peptide action on DNA synthesis and cell survival was ascertained
Ubiquity of OGF-OGFr axis in thyroid follicular cell-derived cancer was assessed in KTC-1 (PTC) and WRO 82-1 (FTC) tumor cells

Results

OGF and OGFr present in KAT-18 cells
Concentrations of 10-6 M OGF inhibited cell replication up to 30%, whereas NTX increased cell growth up to 35% relative to cultures treated with sterile water
OGF treatment reduced cell number by as much as 38% in KAT-18 ATC in a dose-dependent and receptor-mediated manner
OGF antibodies neutralized the inhibitory effects of OGF, and siRNA knockdown of OGFr negated growth inhibition by OGF
Cell survival was not altered by OGF, but DNA synthesis as recorded by BrdU incorporation was depressed by 28% in OGF-treated cultures compared to those exposed to sterile water
OGF-OGFr axis detected and functional in PTC (KTC-1) and FTC (WRO 82-1) cell lines

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