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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2016.10
- 수록면
- 400 - 408 (9page)
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초록· 키워드
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Background: Ginsenoside Rh2 (GRh2) is the main bioactive component in American ginseng, a commonly used herb, and its antitumor activity had been studied in previous studies. PDZ-binding kinase/T-LAK cell-originated protein kinase (PBK/TOPK), a serine/threonine protein kinase, is highly expressed in HCT116 colorectal cancer cells.
Methods: We examined the effect of GRh2 on HCT116 cells ex vivo. Next, we performed in vitro binding assay and in vitro kinase assay to search for the target of GRh2. Furthermore, we elucidated the underlying molecular mechanisms for the antitumor effect of GRh2 ex vivo and in vivo.
Results: The results of our in vitro studies indicated that GRh2 can directly bind with PBK/TOPK and GRh2 also can directly inhibit PBK/TOPK activity. Ex vivo studies showed that GRh2 significantly induced cell death in HCT116 colorectal cancer cells. Further mechanistic study demonstrated that these compounds inhibited the phosphorylation levels of the extracellular regulated protein kinases 1/2 (ERK1/2) and (H3) in HCT116 colorectal cancer cells. In vivo studies showed GRh2 inhibited the growth of xenograft tumors of HCT116 cells and inhibited the phosphorylation levels of the extracellular regulated protein kinases 1/2 and histone H3.
Conclusion: The results indicate that GRh2 exerts promising antitumor effect that is specific to human HCT116 colorectal cancer cells through inhibiting the activity of PBK/TOPK.
Methods: We examined the effect of GRh2 on HCT116 cells ex vivo. Next, we performed in vitro binding assay and in vitro kinase assay to search for the target of GRh2. Furthermore, we elucidated the underlying molecular mechanisms for the antitumor effect of GRh2 ex vivo and in vivo.
Results: The results of our in vitro studies indicated that GRh2 can directly bind with PBK/TOPK and GRh2 also can directly inhibit PBK/TOPK activity. Ex vivo studies showed that GRh2 significantly induced cell death in HCT116 colorectal cancer cells. Further mechanistic study demonstrated that these compounds inhibited the phosphorylation levels of the extracellular regulated protein kinases 1/2 (ERK1/2) and (H3) in HCT116 colorectal cancer cells. In vivo studies showed GRh2 inhibited the growth of xenograft tumors of HCT116 cells and inhibited the phosphorylation levels of the extracellular regulated protein kinases 1/2 and histone H3.
Conclusion: The results indicate that GRh2 exerts promising antitumor effect that is specific to human HCT116 colorectal cancer cells through inhibiting the activity of PBK/TOPK.
목차
ABSTRACT
1. Introduction
2. Materials and methods
3. Results
4. Discussion
References
참고문헌 (41)
참고문헌 신청
[학술지(정기간행물)] - Abe Y / 2000 / Cloning and expression of a novel MAPKK-like protein kinase, lymphokine-activated killer T-cell-originated protein kinase, specifically expressed in the testis and activated lymphoid cells / J Biol Chem 275 : 21525 ~ 21531
[학술지(정기간행물)] - Gaudet S / 2000 / Characterization of PDZ-binding kinase, a mitotic kinase / Proc Natl Acad Sci U S A 97 : 5167 ~ 5172
[학술지(정기간행물)] - Matsumoto S / 2004 / Characterization of a MAPKK-like protein kinase TOPK / Biochem Biophys Res Commun 325 : 997 ~ 1004
[학술지(정기간행물)] - Ayllón V / 2007 / PBK/TOPK promotes tumour cell proliferation through p38 MAPK activity and regulation of the DNA damage response / Oncogene 26 : 3451 ~ 3461
[학술지(정기간행물)] - Oh SM / 2007 / T-lymphokine-activated killer cell-originated protein kinase functions as a positive regulator of c-Jun-NH2-kinase 1 signaling and H-Ras-induced cell transformation / Cancer Res 67 : 5186 ~ 5194
[학술지(정기간행물)] - Gaudet S / 2000 / Characterization of PDZ-binding kinase, a mitotic kinase / Proc Natl Acad Sci U S A 97 : 5167 ~ 5172
[학술지(정기간행물)] - Matsumoto S / 2004 / Characterization of a MAPKK-like protein kinase TOPK / Biochem Biophys Res Commun 325 : 997 ~ 1004
[학술지(정기간행물)] - Ayllón V / 2007 / PBK/TOPK promotes tumour cell proliferation through p38 MAPK activity and regulation of the DNA damage response / Oncogene 26 : 3451 ~ 3461
[학술지(정기간행물)] - Oh SM / 2007 / T-lymphokine-activated killer cell-originated protein kinase functions as a positive regulator of c-Jun-NH2-kinase 1 signaling and H-Ras-induced cell transformation / Cancer Res 67 : 5186 ~ 5194
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UCI(KEPA) : I410-ECN-0101-2018-524-001598532