title: Id1 promotes lung cancer cell proliferation and tumor growth through Akt-related pathway.
abstract: Overexpression of Id family proteins inhibits cell differentiation and enhances cell proliferation and invasiveness. Although Id1 is the Id family member mostly linked to tumorigenesis, its role in lung cancer is unclear. An elevated Id1 expression was observed in lung cancer cell lines as well as lung cancer tissues. Id1 overexpression increased cell proliferation while Id1 knockdown decreased cell proliferation, mostly through Akt-related pathway. Nude mice study further confirmed an increased tumor growth in Id1-overexpressing cells and a decreased tumor growth in Id1-knockdowned cells. In conclusion, inactivation of Id1 may provide a novel strategy for treatment of lung cancer patients.
authors.affiliation: Division of Thoracic Surgery, Department of Surgery, E-DA Hospital, No. 1 E-DA Road, Jiau-Shu, Kaohsiung 824, Taiwan, ROC.
authors.forename: Yu-Jen
authors.initials: YJ
authors.lastname: Cheng
authors.forename: Jen-Wei
authors.initials: JW
authors.lastname: Tsai
authors.forename: Kun-Chou
authors.initials: KC
authors.lastname: Hsieh
authors.forename: Yu-Chi
authors.initials: YC
authors.lastname: Yang
authors.forename: Yun-Ju
authors.initials: YJ
authors.lastname: Chen
authors.forename: Ming-Shyang
authors.initials: MS
authors.lastname: Huang
authors.forename: Shyng-Shiou
authors.initials: SS
authors.lastname: Yuan
mesh_terms: D000818:Animals; D001483:Base Sequence; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D017931:DNA Primers; D055785:Gene Knockdown Techniques; D006801:Humans; D051798:Inhibitor of Differentiation Protein 1 / Q000235:genetics / Q000502:physiology*; D008175:Lung Neoplasms / Q000201:enzymology / Q000473:pathology*; D051379:Mice; D008807:Mice, Inbred BALB C; D008819:Mice, Nude; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*
chemical_list: D017931:DNA Primers; C497453:ID1 protein, human; D051798:Inhibitor of Differentiation Protein 1; D051057:Proto-Oncogene Proteins c-akt