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  • Xia, Dianren  (5)
  • 2010-2014  (5)
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  • 2010-2014  (5)
Year
Subjects(RVK)
  • 1
    Online Resource
    Online Resource
    Human Enhancer of Filamentation 1 Is a Mediator of Hypoxia-Inducible Factor-1α–Mediated Migration in Colorectal Carcinoma Cells
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Research Vol. 70, No. 10 ( 2010-05-15), p. 4054-4063
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 10 ( 2010-05-15), p. 4054-4063
    Abstract: Human enhancer of filamentation 1 (HEF1; also known as NEDD9 or Cas-L) is a scaffolding protein that is implicated in regulating diverse cellular processes, such as cellular attachment, motility, cell cycle progression, apoptosis, and inflammation. Here, we identify HEF1 as a novel hypoxia-inducible factor-1α (HIF-1α)–regulated gene and reveal that HEF1 mediates hypoxia-induced migration of colorectal carcinoma cells. HEF1 is highly expressed in cultured colorectal carcinoma cells exposed to hypoxia and in the hypoxic areas of human colorectal cancer (CRC) specimens. Moreover, our data show that HIF-1α mediates the effects of hypoxia on induction of HEF1 expression via binding to a hypoxia-responsive element of the HEF1 promoter. Importantly, the induction of HEF1 expression significantly enhances hypoxia-stimulated HIF-1α transcriptional activity by modulating the interaction between HIF-1α and its transcriptional cofactor p300. Inhibition of HEF1 expression also reduced the levels of hypoxia-inducible genes, including those that regulate cell motility. Cell migration was reduced dramatically following knockdown of HEF1 expression under hypoxic conditions. Thus, this positive feedback loop may contribute to adaptive responses of carcinoma cells encountering hypoxia during cancer progression. Cancer Res; 70(10); 4054–63. ©2010 AACR.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-09-2110
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
    Location Call Number Limitation Availability
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    Online Resource
  • 2
    Online Resource
    Online Resource
    HEF1 Is a Crucial Mediator of the Proliferative Effects of Prostaglandin E2 on Colon Cancer Cells
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Research Vol. 70, No. 2 ( 2010-01-15), p. 824-831
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 2 ( 2010-01-15), p. 824-831
    Abstract: Prostaglandin E2 (PGE2), one of the downstream products of cyclooxygenase-2 enzymatic activity, promotes colorectal carcinogenesis in part by stimulating cell division. In this study, we define a critical mechanism in this process by showing that the prometastatic adapter protein human enhancer of filamentation 1 (HEF1; NEDD9) links PGE2 to the cell cycle machinery in colorectal cancer cells. PGE2 rapidly induced expression of HEF1 mRNA and protein in colorectal cancer cells. HEF1 overexpression elicited the same effects as PGE2 treatment on cell proliferation, cell cycle progression, and tumor growth. Conversely, HEF1 knockdown suppressed PGE2-driven cell proliferation and cell cycle progression. Cell cycle alterations involved HEF1 fragmentation as well as co-distribution of HEF1 and cell cycle kinase Aurora A along spindle asters during cell division. Moreover, Aurora A co-immunoprecipitated with HEF1 and was activated by HEF1. Consistent with a role for HEF1 in colorectal carcinogenesis, we found elevated expression of HEF1 expression in 50% of human colorectal cancers examined, relative to paired normal tissues. These findings establish that PGE2 induces HEF1 expression, which in turn promotes cell cycle progression through its interaction with and activation of Aurora A. Further, they establish that HEF1 is a crucial downstream mediator of PGE2 action during colorectal carcinogenesis. Cancer Res; 70(2); 824–31
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-09-2105
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
    Location Call Number Limitation Availability
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    Online Resource
  • 3
    Online Resource
    Online Resource
    Abstract B39: Prostaglandin E2 induces human enhancer of filamentation 1 to promote the cell motility of colorectal carcinoma cells
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Prevention Research Vol. 3, No. 1_Supplement ( 2010-01-07), p. B39-B39
    Details
    In: Cancer Prevention Research, American Association for Cancer Research (AACR), Vol. 3, No. 1_Supplement ( 2010-01-07), p. B39-B39
    Abstract: PGE2 promotes cell motility during colorectal carcinogenesis. The mechanism by which PGE2 signaling regulates cell motility is not completely understood. Here, we demonstrated that PGE2 treatment induces HEF1 expression that links with cell motility in colorectal cancer cells. PGE2 rapidly stimulated HEF1 expression in colorectal cancer cells. Both PGE2 treatment and HEF1 overexpression activated Rac 1 and resulted in similar effects on cell spreading. Moreover, knockdown of HEF1 using shRNA suppressed PGE2-driven cell spreading. PKA activator forskolin induced HEF1 expression and cell spreading in a similar manner as PGE2. Inhibition of PKA activity by H-89 attenuated HEF1 expression induced by PGE2. Furthermore, PKA knockdown by siRNA blocked the HEF1 expression and cell spreading induced by PGE2. These data suggest that PGE2 induces HEF1 expression to promote cell motility through a PKA-involved pathway. Citation Information: Cancer Prev Res 2010;3(1 Suppl):B39.
    Type of Medium: Online Resource
    ISSN: 1940-6207 , 1940-6215
    URL: Article
    DOI: 10.1158/1940-6207.PREV-09-B39
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
    detail.hit.zdb_id: 2422346-3
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    Online Resource
  • 4
    Online Resource
    Online Resource
    Abstract 5298: Human enhancer of filamentation 1 induction by Prostaglandin E2 enhances the cell motility of colorectal cancer cells
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Research Vol. 70, No. 8_Supplement ( 2010-04-15), p. 5298-5298
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. 5298-5298
    Abstract: Prostaglandin (PG) E2 promotes cell motility during colorectal carcinogenesis. The mechanism by which PGE2 signaling regulates cell motility is not completely understood. Here, we demonstrated that PGE2 treatment induces HEF1 expression that links with cell motility in colorectal cancer cells. PGE2 rapidly stimulated HEF1 expression in colorectal cancer cells. Both PGE2 treatment and HEF1 overexpression activated Rac 1 and resulted in similar effects on cell spreading. Moreover, knockdown of HEF1 using shRNA suppressed PGE2-driven cell spreading. PKA activator forskolin induced HEF1 expression and cell spreading in a similar manner as PGE2. Inhibition of PKA activity by H-89 attenuated HEF1 expression induced by PGE2. Furthermore, PKA knockdown by siRNA blocked the HEF1 expression and cell spreading induced by PGE2. These data suggest that PGE2 induces HEF1 expression to promote cell motility through a PKA-involved pathway. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 5298.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM10-5298
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
    Location Call Number Limitation Availability
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    Online Resource
  • 5
    Online Resource
    Online Resource
    Abstract 465: Human enhancer of filamentation 1 is a mediator of hypoxia-inducible factor-1 alpha-mediated migration in colorectal carcinoma cells
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Research Vol. 70, No. 8_Supplement ( 2010-04-15), p. 465-465
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. 465-465
    Abstract: Human enhancer of filamentation 1 (HEF1, also known as NEDD9 or Cas-L) is a scaffolding protein that is implicated in regulating diverse cellular processes, including cellular attachment, motility, cell cycle progression, apoptosis and inflammation. Here, we identify HEF1 as a novel hypoxia-inducible factor-1α (HIF-1α) regulating gene and reveal that HEF1 mediates hypoxia-induced migration of colorectal cancer (CRC) cells. Moreover, we found that HIF-1α binds to a hypoxia-responsive element (HRE) of the HEF1 promoter to activate its transcription under hypoxic conditions. We further demonstrate that inhibition of HIF-1α expression abolished hypoxia-induced HEF1 expression and promoter activity in CRC cells. Importantly, silencing of HEF1 significantly inhibited hypoxia-stimulated HIF-1α transcriptional activity by preventing the interaction between HIF-1α and the transcriptional coactivator p300. HEF1 silencing also reduced the expression of hypoxia-inducible genes including those regulating cell motility and inhibited cell migration under hypoxic conditions. Thus, the positive feedback loop may contribute to adaptive responses by CRC cells that encounter hypoxia during CRC progression. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 465.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM10-465
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
    Location Call Number Limitation Availability
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    Online Resource
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