作者: Haruhiko Sugimura , Hitoshi Kitamura , Koji Okudela , Takuya Yazawa , Jun Ishii
DOI: 10.2353/AJPATH.2009.080571
关键词: Cancer cell 、 Somatic cell 、 Cancer 、 Gene silencing 、 Carcinogenesis 、 Mutation 、 Lung cancer 、 Cancer research 、 Biology 、 DNA methylation 、 Pathology 、 Pathology and Forensic Medicine
摘要: FXYD3 is a FXYD-containing Na,K-ATPase ion channel regulator first identified as protein overexpressed in murine breast tumors initiated by oncogenic ras or neu. However, our preliminary study revealed that expression was down-regulated KRAS-transduced airway epithelial cells. This contradiction led us to investigate the role of carcinogenesis lung. mRNA and levels were lower most lung cancer cell lines than either noncancerous tissue Protein also considerable proportion primary cancers nontumoral epithelia; decreased parallel with dedifferentiation process. Also, somatic point mutation, g55c (D19H), found one line. Forced wild-type FXYD3, but not mutant, restored well-demarcated distribution cortical actin cells had lost expression, suggesting plays maintenance cytoskeletal integrity. no association between its promoter's methylation status observed. Therefore, inactivation through gene mutation unknown mechanism could be cause atypical shapes play potential progression cancer.