Withaferin A, a steroidal lactone from Withania somnifera, induces mitotic catastrophe and growth arrest in prostate cancer cells
Roy RV, Suman S, Das TP, Luevano JE, Damodaran C
Journal of natural products · 76 citas
Etiquetas de revisión
Solo mecanismosDatos neutrales que nuestra revisión registró sobre cómo se hizo este estudio. Describen el método, nunca si nos gusta el resultado.
Cómo se estudió
- Diseño
- Estudio in vitro o de mecanismos (clasificado por nuestro filtro de IA)
- Estudiado en
- Células o muestras de laboratorio
- Resultado principal
- Solo mecanismos
Quién lo pagó
- Financiación
- Financiación independiente
- Gobierno
- National Cancer Institute
- Gobierno
- NCI NIH HHS
- Subvenciones
- National Cancer Institute (R01 CA185972); National Cancer Institute (R01CA138797); National Cancer Institute (R01 CA140605)
Según 2 financiadores declarados.
Publicación
- Publicado
- 2013-09-30 · J Nat Prod · vol. 76 · número 10 · págs. 1909–1915
- Editorial
- American Chemical Society
- Citado
- 101 citas · más que el 100% de estudios similares · 27.3× el promedio de su campo
- Impacto
- Entre el 10 % más citado de su campo
- Referencias
- 36 trabajos
- Acceso
- Acceso abierto (copia en repositorio)
- Áreas de investigación
- Phytochemicals and Medicinal Plants · PARP inhibition in cancer therapy · Cell death mechanisms and regulation
- Palabras clave
- Withaferin A, Prostate cancer, Mitotic catastrophe, Cancer research, Cell cycle, Cell cycle checkpoint, Mitosis, Cell growth, Cancer cell, Cancer, Cyclin-dependent kinase 1, Biology, Withania somnifera, Chemistry, Medicine, Internal medicine, Cell biology, Biochemistry, Pathology
- MeSH
- humans, withania, prostatic neoplasms, cdc2 protein kinase, cyclins, histones, cell cycle, cell division, mitosis, g2 phase, apoptosis, molecular structure, male, tumor suppressor protein p53, cyclin-dependent kinase inhibitor p21, withanolides, protein serine-threonine kinases
5 autores
- Ram Vinod Roy🇺🇸Texas Tech University; The University of Texas at El Paso; Texas Tech University Health Sciences Center
- Suman Suman🇺🇸Texas Tech University; Texas Tech University Health Sciences Center
- Trinath Prasad Das🇺🇸Texas Tech University; Texas Tech University Health Sciences Center
- Joe E. Luevano🇺🇸Texas Tech University; Texas Tech University Health Sciences Center
- Chendil Damodaran🇺🇸 · autor de correspondenciaTexas Tech University; Texas Tech University Health Sciences Center
Resumen
El texto original del estudio, en el idioma en que se publicó.
Cell cycle deregulation is strongly associated with the pathogenesis of prostate cancer. Clinical trials of cell cycle regulators that target either the G0/G1 or G2/M phase to inhibit the growth of cancers including prostate cancer are increasing. The present study focused on the cell cycle regulatory potential of the withanolide withaferin A (1) on prostate cancer cells. Compound 1 induced G2/M arrest in both prostate cancer cell lines (PC-3 and DU-145) when treated for 48 h. The G2/M arrest was accompanied by upregulation of phosphorylated Wee-1, phosphorylated histone H3, p21, and Aurora B. On the other hand, downregulation of cyclins (A2, B1, and E2) and a reduction in phosphorylated Cdc2 (Tyr15) were observed in 1-treated prostate cancer cells. In addition, decreased levels of phosphorylated Chk1 (Ser345) and Chk2 (Thr68) were evident in prostate cancer cells on treatment with 1. These results suggest that activation of Cdc2 leads to arrest in the M phase, with abnormal duplication, and initiation of mitotic catastrophe that results in cell death. In conclusion, these results show clearly the potential of 1 as a regulator of the G2/M phase of the cell cycle and as a therapeutic agent for prostate cancer.
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