Abstract
IntroductionMilk secretion is stimulated by prolactin, a hormone secreted from anterior pituitary gland. It is known that prolactin could lead breast and prostate cancer progression. Recent reports point out the concentration of serum prolactin in non small cell lung cancer (NSCLC) patients were significantly higher than health people. The patients with higher concentration of serum prolactin have lower survival rate than normal level on serum prolactin patients. PRL receptor (PRLR) expression level, however, was not relatived to paitients’ survival rate. It is unclear whether prolactin promoted lung cancer progression and the action mechanism of prolactin in lung cancer.Material and methodsCells were seeded in 96 well plate with complete medium. After 24 hour of plating, cells were serum starved for 16 hour and then treatment with PRL. MTT assay was applied for cell proliferation. The protein level of JAK2/STAT3 and VEGF were determined by western blot. The mRNA level was measured by quantitative real time polymerase chain reaction (q-PCR).Results and discussionsOur data show that prolactin promoted cell proliferation in NSCLC cells. Expressed growth hormone receptor (GHR), not prolactin receptor (PRLR), was observed in all NSCLC cell lines. Increased expression of p-JAK2 and p-STAT3 were found in cells treated with prolactin. Treatment with prolactin also increased STAT3-regulated downstream gene VEGF mRNA and protein expressions. In contrast, the protein expression of p-JAK2 was decreased after inhibition of GHR.ConclusionProlactin binds to and activates GHR downstream signalling pathway JAK2/STAT3. Activated STAT3 translocates to nucleus and increases downstream gene VEGF transcription activity. Also, prolactin promotes cell proliferation and VEGF expression in NSCLC cells.
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