Abstract
The role of cadmium with respect to cell growth is still under debate. Low concentration of cadmium was applied to mice primary lung epithelial cells and cell proliferation was measured both by cell cycle analysis and Brdu incorporation assay, effects of different dose of cadmium on lung epithelial cells was evaluated morphologically by atomic force microscopy. RT-PCR and western blot confirmed the specific signalling pathways regarding cadmium induced lung cell proliferation. Primary lung epithelial cells were transfected with siEGFR and molecular interactions of downstream signalling molecules were determined. We have reported RNAi induced silencing of the EGFR, which is over expressed in cadmium induced primary mouse lung epithelial cells. siEGFR effectively prevents expression of proinflammatory and cell proliferative markers. Moreover N-acetyl cysteine mediated inhibition of EGFR and downstream signalling molecules indicate the involvement of reactive oxygen species induced up regulation of EGFR by lower dose of cadmium. We have evaluated how exposure to low concentration of cadmium promotes the growth of primary mice lung epithelial cell by EGFR signalling. We have also transfected the primary lung epithelial cell with siRNA against the regulatory subunit of nuclear factor κβ (NF-κβ) and the data shows that cadmium induced lung cell proliferation is the effect of EGFR mediated NF-κβ activation.
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