Prolactin receptor isoforms expression and activation of STAT5 in lung cancer cell lines: its possible association with carcinogenesis

Background In the last years, it has been noticed the participation of prolactin in different malignancies such as breast and prostate cancer. Recently, prolactin (PRL) was proposed as a biomarker for lung cancer but its molecular mechanisms remain to be explored in this tissue. The aim of this work was to assess prolactin receptor (PRLR) isoforms expression in lung cell lines and its effects in cell viability, proliferation and pathways activation in normal and lung cancer cell lines. Methods and Results PRLR was assessed by WB and immunofluorescence, cell proliferation was performed using MTT assay and STAT5 activation was assessed using WB to detect p-STAT5 and immunofluorescence to explore p-STAT5 nuclear translocation. We found differential expression of PRLR isoforms which were localized differentially in cellular compartments in lung cancer cell lines A549 and SK-LU-1 and in the normal lung cell line BEAS-2B. We did not observe significant differences in cell viability after PRL administration at low doses, however, an augmented viability was found at high doses of PRL treatment. Importantly, at low doses of PRL, we observed an increase in p-STAT5 and its translocation to the nucleus. Conclusions The overall results suggest that PRL may play a differential role in lung cancer cells via STAT5 activation by using different PRLR isoforms. However, further studies are needed to stablish its role in lung carcinogenesis.