Abstract | BACKGROUND:
Renieramycin M, has been shown to exhibit promising anticancer activity against some cancer cell lines; however, the underlying mechanism remains unknown. MATERIALS AND METHODS: RESULTS:
Renieramycin M treatment caused p53 activation, which subsequently down-regulated anti-apoptotic MCL-1 and BCL-2 proteins, while the level of pro-apoptotic BAX protein was not altered. The subtoxic concentrations of renieramycin M significantly decreased invasion and migration abilities of cancer cells. In addition, this compound showed a strong inhibitory effect on anchorage-independent growth of the cells. CONCLUSION:
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Authors | Hasseri Halim, Preedakorn Chunhacha, Khanit Suwanborirux, Pithi Chanvorachote |
Journal | Anticancer research
(Anticancer Res)
Vol. 31
Issue 1
Pg. 193-201
(Jan 2011)
ISSN: 1791-7530 [Electronic] Greece |
PMID | 21273598
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Alkaloids
- Myeloid Cell Leukemia Sequence 1 Protein
- Proto-Oncogene Proteins c-bcl-2
- TP53 protein, human
- Tetrahydroisoquinolines
- Tumor Suppressor Protein p53
- renieramycin M
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Topics |
- Alkaloids
(pharmacology)
- Animals
- Anoikis
(drug effects)
- Apoptosis
(drug effects)
- Blotting, Western
- Carcinoma, Non-Small-Cell Lung
(drug therapy, metabolism, pathology)
- Cell Adhesion
(drug effects)
- Cell Movement
(drug effects)
- Cell Proliferation
(drug effects)
- Colony-Forming Units Assay
- Humans
- Lung Neoplasms
(drug therapy, metabolism, pathology)
- Myeloid Cell Leukemia Sequence 1 Protein
- Porifera
(chemistry)
- Proto-Oncogene Proteins c-bcl-2
(metabolism)
- Tetrahydroisoquinolines
(pharmacology)
- Tumor Cells, Cultured
- Tumor Suppressor Protein p53
(metabolism)
- Wound Healing
(drug effects)
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