Involvement of Met receptor pathway in aggressive behavior of colorectal cancer cells induced by parathyroid hormone-related peptide

Figure 1 Parathyroid hormone-related peptide modulates the protein expression of Met receptor in HCT116 cells. Cells were treated with or without 10^-8 mol/L parathyroid hormone-related peptide (PTHrP) for different times. The protein levels of pro-Met (Met precursor) and Met [tyrosine kinase receptor (RTK) mature form] were analyzed by Western blot to investigate whether the molecular mechanisms trigged by PTHR type 1 (PTHR1) after binding of PTHrP are capable of modulating the expression of the mature form of the RTK Met in HCT116 cells. GAPDH protein levels were determined as a control of the amount of proteins present in the membrane, since this protein is not substantially modified with the treatment by the cytokine. Graph bars represent the average of the results obtained from three independent experiments. GAPDH: Glyceraldehyde 3-phosphate dehydrogenase; Met: Receptor tyrosine kinase Met; PTHrP: Parathyroid hormone-related peptide. ^aP < 0.05; ^bP < 0.01.