2013 Fiscal Year Final Research Report
Elucidation of the molecular mechanisms of early breast cancer invasion and metastasis
| Project/Area Number |
23590323
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
General medical chemistry
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| Research Institution | Hokkaido University |
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Principal Investigator |
HASHIMOTO Ari 北海道大学, 医学(系)研究科(研究院), 助教 (60390803)
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| Project Period (FY) |
2011 – 2013
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| Keywords | 浸潤 / 転移 / Arf6 / GEP100 / EMT / p53 |
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| Research Abstract |
Cancer progression by which epithelial tumor cells acquire a more motile and invasive phenotype has been closely linked to the epithelial-mesenchymal transition (EMT) process. We found that GEP100-Arf6-AMAP1 pathway is important for acquisition of mesenchymal invasive phenotypes of breast cancers and TP53 alterations link to this process. Metabolic pathway regulated by mutant p53 is required for Arf6 activation. The clinical specimens of human breast cancer showed that the expression of GEP100-Arf6-AMAP1 signal correlated with recurrence after radiotherapy. Database analysis also showed that co-incidence of TP53 mutations and the high expression of this signal pathway statistically correlate with poor survival. These results suggest that generation of the Arf6-based mesenchymal invasive pathway by TP53 alterations regulate malignant progression and appears to be crucial for poor prognosis in breast cancer.
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Research Products
(20 results)
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[Journal Article] Co-overexpression of GEP100 and AMAP1 proteins correlates with rapid local recurrence after breast conservative therapy2013
Author(s)
Kinoshita R., Nam J.M., Ito Y.M., Hatanaka K.C., Hashimoto A., Handa H., OtsukaY., Hashimoto S., Onodera Y., Hosoda M., Onodera S., Shimizu S., Tanaka S., Shirato H., Tanino M., Sabe H.
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Journal Title
PLoS One
Volume: 8
Pages: e76791
Peer Reviewed
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[Journal Article] GEP100-Arf6-AMAP1-cortactin pathway frequently used in cancer invasion is activated by VEGFR2 to promote angiogenesis2011
Author(s)
Hashimoto A., Hashimoto S., Ando R., Noda K., Ogawa E., Kotani H., Hirose M., Menju T., Morishige M., Manabe T., Toda Y., Ishida S., and Sabe H.
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Journal Title
PLoS One
Volume: 6
Pages: e23359
Peer Reviewed
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[Presentation] Mechanisms by which p53 alterations generate GEP100-Arf6-AMAP1 pathway as a mesenchymal invasion machinery to be activated by external ligands2013
Author(s)
Hashimoto A., Hashimoto S., Onodera Y., Oikawa T., Oneyama C., Kinoshita R., Nam J.M., Tanino M., Sugino H., Yoshikawa A., Otsuka Y., Handa H., Yoshino M., Sato H., Fukuda S., Tanaka S., Shirato H., Ito Y., Okada M., Sabe H.
Organizer
第36回日本分子生物学会年会
Place of Presentation
神戸
Year and Date
2013-12-04
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[Presentation] Mutant-p53 generates the GEP100-Arf6-AMAP1 pathway to promote breast cancer invasiveness2013
Author(s)
Hashimoto S., Hashimoto A., Oneyama C., Yoshikawa A., Sugino H., Handa H., Yoshino M., Otsuka Y., Onodera Y., Okada M., Sabe H.
Organizer
第86回日本生化学大会
Place of Presentation
横浜
Year and Date
2013-09-12
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[Presentation] Mutant-p53 generates GEP100-Arf6-AMAP1-EPB41L5 pathway externally activated to promote mesenchymal invasion2013
Author(s)
Hashimoto A., Hashimoto S., Oneyama C., Onodera Y., Sugino H., Yoshikawa A., Otsuka Y., Handa H., Okada M., Sabe H.
Organizer
The First International Meeting, Epithelial Tubulology
Place of Presentation
札幌
Year and Date
2013-06-23
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[Presentation] Mutant-p53 generates GEP100-Arf6-AMAP1 pathway to be activated by TGFβ1 and receptor tyrosine kinases to promote cancer invasion.2012
Author(s)
Hashimoto A., Hashimoto S., Yoshikawa A., Sugino H., Handa H., Kinoshita R., Hatanaka K.C., Mikami S., Tanino M., Mito S., Sato H., Otsuka Y., Yoshino H., Kado Y., Nam J.M., Onodera Y., Tanaka S., Shirato H., Sabe H.
Organizer
第35回日本分子生物学会年会
Place of Presentation
福岡
Year and Date
2012-12-12
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[Presentation] Mutant-p53 generates GEP100-Arf6-AMAP1 pathway to promote breast cancer cell invasiveness in response to TGFβ12012
Author(s)
Hashimoto A., Hashimoto S., Yoshikawa A., Sugino H., Handa H., Mito S., Sato H., Otsuka Y., Yoshino H., Nam J.M., Onodera Y., Sabe H.
Organizer
第71回日本癌学会学術総会
Place of Presentation
札幌
Year and Date
2012-09-20
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[Presentation] MUTANT-p53 GENERATES GEP100-Arf6-AMAP1 PATHWAY TO PROMOTE BREAST CANCER CELL INVASIVENESS IN RESPONSE TO TGFβ12012
Author(s)
Hashimoto A., Hashimoto S., Yoshikawa A., Sugino H., Handa H., Mito S., Sato H., Otsuka Y., Yoshino H., Nam J.M., Onodera Y., Sabe H.
Organizer
The31th Sapporo International Cancer Symposium
Place of Presentation
札幌
Year and Date
2012-06-23
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[Presentation] HGFR/c-Met-mediated activation of GEP100-Arf6-AMAP1 pathway is an integral part for TGFβ-induced cancerous EMT and invasiveness2011
Author(s)
Hashimoto A., Hashimoto S., Otsuka Y., Handa H., Sato H., Sugino H., Yoshikawa A., Umemoto T., Onodera Y., Fukuda S., Sabe H.
Organizer
第63回日本細胞生物学会大会
Place of Presentation
札幌
Year and Date
20110628-29
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[Presentation] Mutant p53 is essential for TGFβ1-induced breast cancer cell invasion via activation of GEP100-Arf6-AMAP1 pathway2011
Author(s)
Hashimoto A. , Hashimoto S., Otsuka Y., Yoshikawa A., Sugino H., Handa H., Sato H., Nam J.M., Shirato H., Fukuda S., Onodera Y., Sabe H.
Organizer
第34回日本分子生物学会年会
Place of Presentation
横浜
Year and Date
2011-12-15
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[Presentation] Mutant p53 is essential for TGFβ1-induced breast cancer cell invasiveness via activation of GEP100-Arf6-AMAP1 pathway2011
Author(s)
Hashimoto A., Hashimoto S., Otsuka Y., Yoshikawa A., Sugino H., Handa H., Nam J.M., Sato H., Fukuda S., Onodera Y., Sabe H.
Organizer
第70回日本癌学会学術総会
Place of Presentation
名古屋
Year and Date
2011-10-03
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