Aurora-A transcriptional silencing and Vincristine treatment show a synergistic effect in human tumor cells

Aldo Di Leonardo, Laura Lentini, Aldo Di Leonardo, Angela Amato, Lavinia Insalaco, Tiziana Schillaci

Risultato della ricerca: Article

14 Citazioni (Scopus)

Abstract

Aurora-A is a centrosome-associated serine/threonine kinase that is overexpressed in multiple types of human tumors. Primarily, Aurora-A functions in centrosome maturation and mitotic spindle assembly. Overexpression of Aurora-A induces centrosome amplification and G(2)/M cell-cycle progression. Recently, it was observed that overexpression of Aurora-A renders cells resistant to cisplatin (CDDP)-, etoposide, and paclitaxel-induced apoptosis. Our results indicate that already in initial stages of cancer progression Aurora-A overexpression could have a major role in inducing supernumerary centrosomes and aneuploidy, as shown by immunohistochemistry on tissue sections from various stages of human colon cancer. Aneuploidy was also observed after Aurora-A ectopic overexpression in colon cancer cells with MIN phenotype. Silencing of Aurora-A by RNA interference in tumor cell lines triggered arrest of the cell cycle associated to apoptosis/mitotic catastrophe. Finally, Aurora-A transcriptional silencing seems to confer cancer cells a greater sensitivity to chemotherapy by vincristine, indicating Aurora-A as a possible gene target in cancer therapy.
Lingua originaleEnglish
pagine (da-a)115-125
Numero di pagine16
RivistaOncology Research
Volume17
Stato di pubblicazionePublished - 2008

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Centrosome
Vincristine
Aneuploidy
Colonic Neoplasms
Neoplasms
Apoptosis
Spindle Apparatus
Protein-Serine-Threonine Kinases
Etoposide
Therapeutics
RNA Interference
Paclitaxel
Cell Cycle Checkpoints
Tumor Cell Line
Cisplatin
Cell Cycle
Immunohistochemistry
Phenotype
Drug Therapy
Genes

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research

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Aurora-A transcriptional silencing and Vincristine treatment show a synergistic effect in human tumor cells. / Di Leonardo, Aldo; Lentini, Laura; Di Leonardo, Aldo; Amato, Angela; Insalaco, Lavinia; Schillaci, Tiziana.

In: Oncology Research, Vol. 17, 2008, pag. 115-125.

Risultato della ricerca: Article

Di Leonardo, Aldo ; Lentini, Laura ; Di Leonardo, Aldo ; Amato, Angela ; Insalaco, Lavinia ; Schillaci, Tiziana. / Aurora-A transcriptional silencing and Vincristine treatment show a synergistic effect in human tumor cells. In: Oncology Research. 2008 ; Vol. 17. pagg. 115-125.
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AU - Di Leonardo, Aldo

AU - Lentini, Laura

AU - Di Leonardo, Aldo

AU - Amato, Angela

AU - Insalaco, Lavinia

AU - Schillaci, Tiziana

PY - 2008

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N2 - Aurora-A is a centrosome-associated serine/threonine kinase that is overexpressed in multiple types of human tumors. Primarily, Aurora-A functions in centrosome maturation and mitotic spindle assembly. Overexpression of Aurora-A induces centrosome amplification and G(2)/M cell-cycle progression. Recently, it was observed that overexpression of Aurora-A renders cells resistant to cisplatin (CDDP)-, etoposide, and paclitaxel-induced apoptosis. Our results indicate that already in initial stages of cancer progression Aurora-A overexpression could have a major role in inducing supernumerary centrosomes and aneuploidy, as shown by immunohistochemistry on tissue sections from various stages of human colon cancer. Aneuploidy was also observed after Aurora-A ectopic overexpression in colon cancer cells with MIN phenotype. Silencing of Aurora-A by RNA interference in tumor cell lines triggered arrest of the cell cycle associated to apoptosis/mitotic catastrophe. Finally, Aurora-A transcriptional silencing seems to confer cancer cells a greater sensitivity to chemotherapy by vincristine, indicating Aurora-A as a possible gene target in cancer therapy.

AB - Aurora-A is a centrosome-associated serine/threonine kinase that is overexpressed in multiple types of human tumors. Primarily, Aurora-A functions in centrosome maturation and mitotic spindle assembly. Overexpression of Aurora-A induces centrosome amplification and G(2)/M cell-cycle progression. Recently, it was observed that overexpression of Aurora-A renders cells resistant to cisplatin (CDDP)-, etoposide, and paclitaxel-induced apoptosis. Our results indicate that already in initial stages of cancer progression Aurora-A overexpression could have a major role in inducing supernumerary centrosomes and aneuploidy, as shown by immunohistochemistry on tissue sections from various stages of human colon cancer. Aneuploidy was also observed after Aurora-A ectopic overexpression in colon cancer cells with MIN phenotype. Silencing of Aurora-A by RNA interference in tumor cell lines triggered arrest of the cell cycle associated to apoptosis/mitotic catastrophe. Finally, Aurora-A transcriptional silencing seems to confer cancer cells a greater sensitivity to chemotherapy by vincristine, indicating Aurora-A as a possible gene target in cancer therapy.

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