Cortactin, an actin-interacting protein, is implicated in cytoskeletal architecture and often amplified in several types of cancer including gastric adenocarcinomas.
The objective was to characterize and associate the receptor reactivities of fibroblastic growth factor (FGF)-2, FGF-7, FGF-8, epidermal growth factor (EGF), α-actin and vimentin in relation to the androgen receptor (AR), α and β estrogen receptors (ERα and ERβ), and prolactin receptor in the prostate of elderly men showing low- and high-grade adenocarcinoma.
Profilin-1 (Pfn1), a ubiquitously expressed actin-binding protein, has gained interest in epithelial-derived cancer because of its downregulation in expression in various adenocarcinoma.
Using immunohistochemistry in a well-characterized set of adenocarcinoma tissues, we showed down-regulation of epithelial markers (E-cadherin and cytokeratin 18) and up-regulation of mesenchymal markers (vimentin and alpha-smooth muscle actin) with concomitant transforming growth factor-beta1 (TGF-beta1) expression at the invasive margin compared with the central tumor.
The OD ratio of GST-Pi mRNA expression to beta-actin mRNA was 1.17+/-0.13 and 1.3+/-0.13 in ADC and SCC samples, respectively, which is significantly higher (P<0.05) than matching control (0.78+/-0.06 and 0.85+/-0.07).
CDX2 and PITX1 messenger RNA (mRNA) expression levels, relative to the control gene beta-actin, were measured by reverse transcription-polymerase chain reaction in specimens of Barrett's IM (n = 21), dysplasia (n = 18), adenocarcinoma (n = 20), and matching normal squamous esophagus tissues (n = 39) collected from 19 patients with Barrett's esophagus and 20 patients with esophageal adenocarcinoma.
We show here that multiple copies of the short actin-binding module CLIK(23) from human or Caenorhabditis elegans calponin proteins effectively inhibit cell motility on two dimensional matrices and suppress soft agar colony formation of metastatic melanoma and adenocarcinoma cells of murine and human origin.