β-Lapachone, a novel Topo I (topoisomerase I) inhibitor, does not stabilize the cleavable complex indicating a novel mode of action, unlike camptothecin (sc-200871). Apoptosis has been demonstrated in HL-60 and human prostate cancer cells treated with β-Lapachone via a p53-independent mechanism and cell cycle arrest at G0/G1,2. β-Lapachone has been observed to accelerate wound healing by increasing cell proliferation in cells such as: keratinocytes, fibroblasts and endothelial while also increasing the migration of fibroblasts and endothelial cells. β-Lapachone has exhibited anti-inflammatory properties by suppressing the NF-κB activation by blocking IκBα degradation and downregulating the ERK, p38 mitogen-activated protein kinase and Akt pathway.
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See how others have used beta-Lapachone. Click on the entry to view the PubMed entry .
PMID: # 17609380
Bey, EA. et al. 2007. An NQO1- and PARP-1-mediated cell death pathway induced in non-small-cell lung cancer cells by beta-lapachone Proc. Natl. Acad. Sci. USA. 104: 11832-11837.
PMID: # 15044484
Lin, MT et al. 2004. Cyr61 expression confers resistance to apoptosis in breast cancer MCF-7 cells by a mechanism of NF-kB-dependent XIAP up-regulation. J Biol Chem.. 279: 24015-23.
PMID: # 12598645
Li, Y. et al. 2003. Selective killing of cancer cells by beta -lapachone: direct checkpoint activation as a strategy against cancer. Proc. Natl. Acad. Sci. U.S.A.. 100: 2674-2678.
PMID: # 9927052
Shiah, SG. et al. 1999. Activation of c-Jun NH2-terminal kinase and subsequent CPP32/Yama during topoisomerase inhibitor beta-lapachone-induced apoptosis through an oxidation-dependent pathway. Cancer Res.. 59: 391-398.
PMID: # 2740334
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