American Association for Cancer Research
Browse
00085472can071522-sup-can_10-15-07_ehata.pdf (61.74 kB)

Supplementary Table 1, Figures 1-3 from Transforming Growth Factor-β Promotes Survival of Mammary Carcinoma Cells through Induction of Antiapoptotic Transcription Factor DEC1

Download (61.74 kB)
journal contribution
posted on 2023-03-30, 17:42 authored by Shogo Ehata, Aki Hanyu, Makoto Hayashi, Hiroyuki Aburatani, Yukio Kato, Makoto Fujime, Masao Saitoh, Keiji Miyazawa, Takeshi Imamura, Kohei Miyazono
Supplementary Table 1, Figures 1-3 from Transforming Growth Factor-β Promotes Survival of Mammary Carcinoma Cells through Induction of Antiapoptotic Transcription Factor DEC1

History

ARTICLE ABSTRACT

Transforming growth factor-β (TGF-β) signaling facilitates tumor growth and metastasis in advanced cancer. In the present study, we identified differentially expressed in chondrocytes 1 (DEC1, also known as SHARP2 and Stra13) as a downstream target of TGF-β signaling, which promotes the survival of breast cancer cells. In the mouse mammary carcinoma cell lines JygMC(A) and 4T1, the TGF-β type I receptor kinase inhibitors A-44-03 and SB431542 induced apoptosis of cells under serum-free conditions. Oligonucleotide microarray and real-time reverse transcription-PCR analyses revealed that TGF-β induced DEC1 in these cells, and the increase of DEC1 was suppressed by the TGF-β type I receptor kinase inhibitors as well as by expression of dominant-negative TGF-β type II receptor. Overexpression of DEC1 prevented the apoptosis of JygMC(A) cells induced by A-44-03, and knockdown of endogenous DEC1 abrogated TGF-β–promoted cell survival. Moreover, a dominant-negative mutant of DEC1 prevented lung and liver metastasis of JygMC(A) cells in vivo. Our observations thus provide new insights into the molecular mechanisms governing TGF-β–mediated cell survival and metastasis of cancer. [Cancer Res 2007;67(20):9694–703]

Usage metrics

    Cancer Research

    Categories

    Keywords

    Licence

    Exports

    RefWorks
    BibTeX
    Ref. manager
    Endnote
    DataCite
    NLM
    DC