research on the potential molecular targets in DNA repair pathway for enhancing chemosensitivity of oral cancer cells
Project/Area Number |
24659902
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Research Category |
Grant-in-Aid for Challenging Exploratory Research
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Allocation Type | Single-year Grants |
Research Field |
Surgical dentistry
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Research Institution | Nara Medical University |
Principal Investigator |
KIRITA TADAAKI 奈良県立医科大学, 医学部, 教授 (70201465)
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Co-Investigator(Kenkyū-buntansha) |
KAJIHARA Atsuhisa 奈良県立医科大学, 医学部, 研究員 (00382317)
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Project Period (FY) |
2012-04-01 – 2014-03-31
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Project Status |
Completed (Fiscal Year 2013)
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Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
Keywords | DNA repair / 5-fluorouracil / BRCA2 / oral cancer / DNA修復 / 口腔がん / 化学療法 / 5-FU |
Research Abstract |
5-FU is widely used in clinical cancer therapy. 5-FU induces DNA double-strand breaks (DSBs). The aim of this study was to learn more about pathways which are involved in the repair of 5-FU-induced DSBs. Cell survival after drug treatment was examined with colony forming assays using Chinese hamster lung fibroblast cells, or Chinese hamster ovary cell lines which are deficient in DSB repair pathways involving the homologous recombination repair-related genes BRCA2 and XRCC2, and the non-homologous end joining repair-related genes DNA-PKcs and Ku80. It was found that BRCA2 was involved in such repair, and might be effectively targeted to inhibit the repair of 5-FU damage. Observations showed that a knockdown of BRCA2 using small interference RNA suppression increased sensitivity to 5-FU in human oral cancer SAS and HSC3 cells. These findings suggest that down regulation of BRCA2 might be useful for sensitizing tumor cells during 5-FU chemotherapy.
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Report
(3 results)
Research Products
(49 results)
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[Journal Article] Depression of p53-independent Akt survival signals in human oral cancer cells bearing mutated p53 gene after exposure to high-LET radiation2012
Author(s)
Nakagawa Y., Takahashi A., Kajihara A., Yamakawa N., Imai Y., Ota I., Okamoto N., Mori E., Noda T., Furusawa Y., Kirita T., Ohnishi T
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Journal Title
Biochem Biophys Res Commun
Volume: 423(4)(Epub)
Pages: 654-60
Related Report
Peer Reviewed
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[Journal Article] Scientific Committee, Japan Society for Oral Tumors General Rules for Clinical and Pathological Studies on Oral Cancer2012
Author(s)
Izumo T., Kirita T., Ariji E., Ozeki S., Okada N., Okabe S., Okazaki Y., Omura K., Kusama M., SatoT., Shinohara M., Shimozato K., and Working Group 1 on the'Guidelines for Clinical and Pathological Studies of Oral Cancer'
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Journal Title
A Synopsis. Japanese Journal of Clinical Oncology
Volume: 42(11)
Pages: 1099-1109
Related Report
Peer Reviewed
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[Journal Article] Depression of p53-independent Akt survival signals in human oral cancer cells bearing mutated p53 gene after exposure to high-LET radiation.2012
Author(s)
Nakagawa Y., Takahashi A., Kajihara A., Yamakawa N., Imai Y., Ota I., Okamoto N., Mori E., Noda T., Furusawa Y., Kirita T., Ohnishi T.
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Journal Title
Biochem Biophys Res Commun
Volume: 423
Pages: 654-660
Related Report
Peer Reviewed
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