In:
Cancer Research, American Association for Cancer Research (AACR), Vol. 71, No. 8_Supplement ( 2011-04-15), p. 3381-3381
Abstract:
Exposure of B(a)P on lung tissue have been implicated in cancer development and its progression. Even though increasing evidences have been reported adversely effects of B(a)P in tumor progression, mechanism by which exposure of Bap on lung cancer cells increases the metastatic potentials still remains unknown. Here, we show that B(a)P triggers a marked morphological changes of Non Small Cell Lung Cancer (NSCLC) cells. These B(a)P-mediated effects are mimicked by decreasing E-cadherin resulting in loosening cell-cell contacts and by increasing Slug expression resulting in inducing epithelial mesenchymal transition (EMT). In case that NCSCLC cell was prolonged exposed to B(a)P, B(a)P-exposed cells showed increasing cell motility and invasion. They correlate with B(a)P-mediated phosphorylations of JNK and p38. And they are reverted by treatment with their inhibitors. In transient transfection analysis, H1299-snail2, constitutively expressing snail2, increased the cell motility and invasion. AhR shRNA effectively suppresses either B(a)P-mediated tumor invasion and induction of snail2. And suppression of E-caherin was found in H1299-snail2. Results of immunohistochemical stain revealed that Slug strongly expressed in invasive foci of Non Small Cell Lung Cancer tissue. Our results suggested that NSCLC cells prolonged exposed to B(a)P increased cell motility and invasiveness via regulation of expression of Sanil2 by exposure of B(a)P on NSCLC cells. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 3381. doi:10.1158/1538-7445.AM2011-3381
Type of Medium:
Online Resource
ISSN:
0008-5472
,
1538-7445
DOI:
10.1158/1538-7445.AM2011-3381
Language:
English
Publisher:
American Association for Cancer Research (AACR)
Publication Date:
2011
detail.hit.zdb_id:
2036785-5
detail.hit.zdb_id:
1432-1
detail.hit.zdb_id:
410466-3
