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FoxM1 regulates transcription of JNK1 to promote the G1/S transition and tumor cell invasiveness

Wang, I-Ching ; Chen, Yi-Ju ; Hughes, Douglas E ; Ackerson, Timothy ; Major, Michael L ; Kalinichenko, Vladimir V ; Costa, Robert H ; Raychaudhuri, Pradip ; Tyner, Angela L ; Lau, Lester F

The Journal of biological chemistry, 25 July 2008, Vol.283(30), pp.20770-8 [Tạp chí có phản biện]

ISSN: 0021-9258 ; PMID: 18524773 Version:1 ; DOI: 10.1074/jbc.M709892200

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  • Nhan đề:
    FoxM1 regulates transcription of JNK1 to promote the G1/S transition and tumor cell invasiveness
  • Tác giả: Wang, I-Ching ; Chen, Yi-Ju ; Hughes, Douglas E ; Ackerson, Timothy ; Major, Michael L ; Kalinichenko, Vladimir V ; Costa, Robert H ; Raychaudhuri, Pradip ; Tyner, Angela L ; Lau, Lester F
  • Chủ đề: Gene Expression Regulation, Enzymologic ; Gene Expression Regulation, Neoplastic ; Forkhead Transcription Factors -- Physiology ; Mitogen-Activated Protein Kinase 8 -- Metabolism
  • Là 1 phần của: The Journal of biological chemistry, 25 July 2008, Vol.283(30), pp.20770-8
  • Mô tả: The Forkhead box M1 (FoxM1) protein is a proliferation-specific transcription factor that plays a key role in controlling both the G(1)/S and G(2)/M transitions through the cell cycle and is essential for the development of various cancers. We show here that FoxM1 directly activates the transcription of the c-Jun N-terminal kinase (JNK1) gene in U2OS osteosarcoma cells. Expression of JNK1, which regulates the expression of genes important for the G(1)/S transition, rescues the G(1)/S but not the G(2)/M cell cycle block in FoxM1-deficient cells. Knockdown of either FoxM1 or JNK1 inhibits tumor cell migration, invasion, and anchorage-independent growth. However, expression of JNK1 in FoxM1-depleted cells does not rescue these defects, indicating that JNK1 is a necessary but insufficient downstream mediator of FoxM1 in these processes. Consistent with this interpretation, FoxM1 regulates the expression of the matrix metalloproteinases MMP-2 and MMP-9, which play a role in tumor cell invasion, through JNK1-independent and -dependent mechanisms in U2OS cells, respectively. Taken together, these findings identify JNK1 as a critical transcriptional target of FoxM1 that contributes to FoxM1-regulated cell cycle progression, tumor cell migration, invasiveness, and anchorage-independent growth.
  • Ngôn ngữ: English
  • Số nhận dạng: ISSN: 0021-9258 ; PMID: 18524773 Version:1 ; DOI: 10.1074/jbc.M709892200

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