PTTG1 attenuates drug-induced cellular senescence

As PTTG1 (pituitary tumor transforming gene) abundance correlates with adverse outcomes in cancer treatment, we determined mechanisms underlying this observation by assessing the role of PTTG1 in regulating cell response to anti-neoplastic drugs. HCT116 cells devoid of PTTG1 (PTTG1(-/-)) exhibited e...

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Veröffentlicht in:	PloS one 2011-08, Vol.6 (8), p.e23754
Hauptverfasser:	Tong, Yunguang, Zhao, Weijiang, Zhou, Cuiqi, Wawrowsky, Kolja, Melmed, Shlomo
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Anthracyclines Antineoplastic Agents - pharmacology Apoptosis Blotting, Western Brain cancer Brain tumors Cancer Cancer therapies Cell cycle Cell growth Cell Line, Tumor Cellular Senescence - drug effects Cellular Senescence - physiology Colon Colon cancer Colonic Neoplasms - drug therapy Colonic Neoplasms - genetics Colonic Neoplasms - pathology Colorectal cancer Cyclin-dependent kinase inhibitor p21 Cyclin-Dependent Kinase Inhibitor p21 - genetics Cyclin-Dependent Kinase Inhibitor p21 - metabolism Damage detection Deoxyribonucleic acid DNA DNA damage DNA repair Dose-Response Relationship, Drug Doxorubicin Doxorubicin - pharmacology Drug therapy Drugs Event-related potentials Female Gene Knockdown Techniques Gene regulation HCT116 Cells Humans Hydroxamic Acids - pharmacology Immunohistochemistry Kinases Medicine Mice Mice, Nude Mitosis Mutation Neoplasm Proteins - genetics Neoplasm Proteins - physiology p53 Protein Phase transitions Pituitary Pituitary gland Pituitary tumor-transforming proteins Promoter Regions, Genetic - genetics Prostate cancer Protein Binding Proteins RNA Interference Securin Senescence Sensitivity analysis Sensitivity enhancement Sp1 protein Sp1 Transcription Factor - genetics Sp1 Transcription Factor - metabolism Thyroid gland Transcription Trichostatin A Tumor proteins Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - metabolism Tumors Xenograft Model Antitumor Assays Xenografts
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Zusammenfassung:	As PTTG1 (pituitary tumor transforming gene) abundance correlates with adverse outcomes in cancer treatment, we determined mechanisms underlying this observation by assessing the role of PTTG1 in regulating cell response to anti-neoplastic drugs. HCT116 cells devoid of PTTG1 (PTTG1(-/-)) exhibited enhanced drug sensitivity as assessed by measuring BrdU incorporation in vitro. Apoptosis, mitosis catastrophe or DNA damage were not detected, but features of senescence were observed using low doses of doxorubicin and TSA. The number of drug-induced PTTG1(-/-) senescent cells increased ∼4 fold as compared to WT PTTG1-replete cells (p
ISSN:	1932-6203 1932-6203
DOI:	10.1371/journal.pone.0023754