[Download] "Modulation of Protein Tyrosine Phosphatase (PTPγ) Signaling by MicroRNA and Ligand Binding" by Shu-Hong Lin " Book PDF Kindle ePub Free
eBook details
- Title: Modulation of Protein Tyrosine Phosphatase (PTPγ) Signaling by MicroRNA and Ligand Binding
- Author : Shu-Hong Lin
- Release Date : January 18, 2013
- Genre: Medical,Books,Professional & Technical,Science & Nature,
- Pages : * pages
- Size : 5263 KB
Description
Protein Tyrosine Phosphatase γ (PTPγ, encoded by PTPRG gene) has been shown to be an estrogen-regulated tumor suppressor in breast cancers. Our current studies focus on mechanisms which are influential in PTPγ in both breast cancer cell line and primary cultured breast cancer cells. In search for the differences in micorRNA (miRNA) profiles among primary cultured human breast cancer cell (CEC) and adjacent normal cell (NAE), we found 24 up-regulated and 1 down-regulated miRNA in CEC. Among the up-regulated miRNAs, miR-141 is predicted to target PTPRG based on sequence and transient transfection of the precursor for miR-141 (pre-miR-141) in triple negative human breastcancer cell line, MDA-MB-231 cells successfully resulted in the down-regulation of PTPRG. Further experiments with 14 pairs of CEC and NAE from patients revealed a moderate negative association (Kendall’s τ = -0.61) in NAE but not CEC. PTPγ belongs to the receptor type phosphatase family, yet its ligand has not been reported until 2010. Members of contactin (CNTN) family, including CNTN3, 4, 5 and 6, were found to bind PTPγ. However, it is still unclear whether CNTN binding is stimulatory or inhibitory to PTPγ activity. Among the four possible ligands, only CNTN3 was found to be present in normal breast cells. In order to evaluate the impact of CNTN3 binding on PTPγ signaling, we used genes regulated by PTPγ as an indicator. Compared with PTPRG expression level, CNTN3/PTPRG ratio has been found to be equally and even better associated with the expression of downstream genes in CEC and NAE in an opposite direction. Such difference in the direction of association has suggested an inhibitory role for CNTN3 binding in terms of PTPγ signaling.