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쏘라페닙은 간암 치료제로 승인된 유일한 약이다. 전세계 암환자들의 인삼추출물 사용이 증가 되고 있지만 쏘라페닙과의 상호작용에 대한 연구는 부족하다. 사람의 간암 세포주와 생쥐 모델을 사용하여 쏘라페닙과 인삼추출물의 약물 상호작용을 알아보고자 하였다. 저농도 인삼추출물 투여시 암세포주의 성장과 pERK (phosphorylation of extracellular signal-regulated kinase)의 증가가 관찰되었고 고농도 투여시 암세포 억제와 pERK 감소가 관찰되었다. 성장 사이클이 없는 세포에서 쏘라페닙의 항암 효과가 감소한 반면 저농도 인삼 투여 시 항암 효능이 증진되어 나타났다. PD98059 (ERK 인산화 억제재)은 효과적으로 ERK 인산화를 억제하여 인삼추출물의 쏘라페닙 감작 작용을 억제시켰다. 생쥐 간암 세포주 모델에서, 저농도 인삼추출물은 다소 암세포 크기를 증가 시켰지만 고농도 투여시 감소시켰다. 그러나, 인삼추출물과 쏘라페닙 동시 투여시 항암 효능은 현저히 증가되었다. 정상조직에서 저농도 인삼에 의해 PERK 증가가 관찰되었으며 이것은 홍삼에 의한 독성 증가와 관련될 것으로 추정되었다. 결론적으로 인삼추출물과 쏘라페닙은 농도에 따라 항암효능을 증가 시킬 수 있음을 보여 주었지만 독성의 가능성도 함께 증가시켰다. 인삼추출물과 쏘라페닙 약물 상호작용에 대한 더 면밀한 연구가 필요할 것으로 보인다.
Sorafenib is the only approved systemic, therapeutic agent for hepatocellular carcinoma (HCC). The use of Ginseng Extract (GE) in cancer patients is growing worldwide; however, drug interaction between sorafenib and GE has not been illuminated. Four different human cancer cell lines including HepG2 were used and immunocompetent mice were implanted subcutaneously with a mouse HCC cell line. Treatment with low dose GE stimulated cell growth, while a high dose inhibited growth. pERK (phosphorylation of extracellular signal-regulated kinase) was concomitantly increased and decreased respective of different doses of GE. Antitumoral effect of sorafenib decreased in non-proliferating phase cells but was sensitized after low dose GE (LDG) treatment. PD98059 (ERK phosphorylation inhibitor) efficiently blocked ERK phosphorylation, resulting in loss of sorafenib sensitization even after LDG treatment. In the HCC mouse model, LDG alone slightly increased tumor size while sorafenib alone significantly decreased it. However, a combination of LDG and sorafenib significantly decreased tumor size compared with sorafenib alone. Increase of pERK was observed in some normal mice organs and mild inflammatory change was observed in some of these organs, suggesting pERK activation by LDG may cause unexpected toxicity in normal cells. GE, dose-dependently, induced stimulation or inhibition in some human cancer cell lines. Combinational use of GE and sorafenib possibly potentiated an antitumoral response to sorafenib. pERK level has been provided as a potential predictive marker for sorafenib. Our result may suggest GE’s dual effects in relation to pERK level in HCC cancer cell lines, and that certain doses of GE can sensitize sorafenib.
Sorafenib is the only approved systemic, therapeutic agent for hepatocellular carcinoma (HCC). The use of Ginseng Extract (GE) in cancer patients is growing worldwide; however, drug interaction between sorafenib and GE has not been illuminated. Four different human cancer cell lines including HepG2 were used and immunocompetent mice were implanted subcutaneously with a mouse HCC cell line. Treatment with low dose GE stimulated cell growth, while a high dose inhibited growth. pERK (phosphorylation of extracellular signal-regulated kinase) was concomitantly increased and decreased respective of different doses of GE. Antitumoral effect of sorafenib decreased in non-proliferating phase cells but was sensitized after low dose GE (LDG) treatment. PD98059 (ERK phosphorylation inhibitor) efficiently blocked ERK phosphorylation, resulting in loss of sorafenib sensitization even after LDG treatment. In the HCC mouse model, LDG alone slightly increased tumor size while sorafenib alone significantly decreased it. However, a combination of LDG and sorafenib significantly decreased tumor size compared with sorafenib alone. Increase of pERK was observed in some normal mice organs and mild inflammatory change was observed in some of these organs, suggesting pERK activation by LDG may cause unexpected toxicity in normal cells. GE, dose-dependently, induced stimulation or inhibition in some human cancer cell lines. Combinational use of GE and sorafenib possibly potentiated an antitumoral response to sorafenib. pERK level has been provided as a potential predictive marker for sorafenib. Our result may suggest GE’s dual effects in relation to pERK level in HCC cancer cell lines, and that certain doses of GE can sensitize sorafenib.
권호기사
참고문헌 (28건) : 자료제공( 네이버학술정보 )
| 번호 | 참고문헌 | 국회도서관 소장유무 |
|---|---|---|
| 1 | Phase II study of sorafenib in patients with advanced hepatocellular carcinoma.  |
미소장 |
| 2 | Alex, A. A., J. R. Molina, S. J. Mandrekar, R. Marks, J. R. Reid, G. Croghan, L. J. Hanson, J. R. Jett, C. Xia, C. Lathia, and R. Simantov. 2007. Phase I trial of sorafenib in combination with gefitinib in patients with refractory or recurrent non-small cell lung cancer. Clin. Cancer Res. 13, 2684-2691. | 미소장 |
| 3 | Chao, Z., Y. Shoyama, and T. Hiroyuki. 2006. Pharmacokinetic study of ginsenosides Rb1 and Rg1 in rat by ELISA using anti-ginsenosides Rb1 and Rg1 monoclonal antibodies. Am. J. Chinese Med. 34, 1069-1081. | 미소장 |
| 4 | Chowdhury, S. J., M. G. Larkin, and M. E. Gore. 2008. Recent advances in the treatment of renal cell carcinoma and the role of targeted therapies. Eur. J. Cancer 44, 2152-2161. | 미소장 |
| 5 | A randomized trial of external beam radiotherapy versus cryoablation in patients with localized prostate cancer |
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| 6 | Complementary and alternative medicine use among women with breast cancer. |
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| 7 | Finn, R. S. 2010. Development of molecularly targeted therapies in hepatocellular carcinoma: where do we go now? Clin. Cancer Res. 16, 390-397. | 미소장 |
| 8 | Asian ginseng enhances the anti-proliferative effect of 5-fluorouracil on human colorectal cancer: Comparison between white and red ginseng | 소장 |
| 9 | Guida, T., S. Anaganti, L. Provitera, R. Gedrich, E. Sullivan, S. M. Wilhelm, M. Santoro, and F. Carlomagno. 2007. Sorafenib inhibits imatinibresistant KIT and platelet-derived growth factor receptor h gatekeeper mutants. Clin. Cancer Res. 13, 3363-3369. | 미소장 |
| 10 | Sorafenib inhibits the imatinib-resistant KITT670I gatekeeper mutation in gastrointestinal stromal tumor. |
미소장 |
| 11 | Sequential Therapy With JX-594, A Targeted Oncolytic Poxvirus, Followed by Sorafenib in Hepatocellular Carcinoma: Preclinical and Clinical Demonstration of Combination Efficacy |
미소장 |
| 12 | Hoshino, R., S. Tanimura, K. Watanabe, T. Kataoka, and M. Kohno. 2001. Blockade of the extracellular signal-regulated kinase pathway induces marked G1 cell cycle arrest and apoptosis in tumor cells in which the pathway is constitutively activated. J. Biochem. 276, 2686-2692. | 미소장 |
| 13 | Sorafenib: a review of its use in advanced hepatocellular carcinoma. |
미소장 |
| 14 | Systemic armed oncolytic and immunologic therapy for cancer with JX-594, a targeted poxvirus expressing GM-CSF. |
미소장 |
| 15 | Koo, H. H., H. J. Jeong, I. Y. Choi, H. J. An, P. D. Moon, S. J. Kim, S. Y. Jee, J. Y. Um, S. H. Hong, S. S. Shin, D. C. Yang, Y. S. Seo, and H. M. Kim. 2007. Mountain grow ginseng induces apoptosis in HL-60 cells and its mechanism have little relation with TNF-alpha production. Am. J. Chinese Med. 35, 169-182. | 미소장 |
| 16 | Panaxadiol, a purified ginseng component, enhances the anti-cancer effects of 5-fluorouracil in human colorectal cancer cells |
미소장 |
| 17 | Ling, Y., L. Yong, and L. Chang-Xiao. 2006. Metabolism and pharmacokinetics of ginsenosides. Asian J. PD and PK. 6, 103-120. | 미소장 |
| 18 | Natural health products that inhibit angiogenesis: a potential source for investigational new agents to treat cancer-Part 1. |
미소장 |
| 19 | The cancer-preventive potential of Panax ginseng: a review of human and experimental evidence |
미소장 |
| 20 | In vitro anti-cancer activity and structure–activity relationships of natural products isolated from fruits of Panax ginseng |
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| 21 | Wang, X. T., J. L. Martindale, and N. J. Holbrook. 2000. Requirement for erk activation in cisplatin-induced apoptosis. J. Biochem. 275, 9435-39443. | 미소장 |
| 22 | BAY 43-9006 exhibits broad spectrum oral antitumor activity and targets the RAF/MEK/ERK pathway and receptor tyrosine kinases involved in tumor progression and angiogenesis. |
미소장 |
| 23 | Ras-mediated activation of ERK by cisplatin induces cell death independently of p53 in osteosarcoma and neuroblastoma cell lines |
미소장 |
| 24 | Yun, T. K. 2001. Panax ginseng–a non-organ-specific cancer preventive? Lancet Oncol. 2, 49-55. | 미소장 |
| 25 | Trial of a new medium-term model using benzo(a)pyrene induced lung tumor in newborn mice. |
미소장 |
| 26 | Yun, T. K., S. H. Kim, and Y. R. Oh. 1987. Medium-term (nine weeks) method for assay of preventive agents against tumor. J. Korean Cancer Assoc. 1-7. | 미소장 |
| 27 | Phosphorylated ERK is a potential predictor of sensitivity to sorafenib when treating hepatocellular carcinoma: evidence from an |
미소장 |
| 28 | Zhu, A. X. Predicting the response to sorafenib in hepatocellular carcinoma: where is the evidence for phosphorylated extracellular signaling-regulated kinase (pERK)? BMC Med. 42. | 미소장 |
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