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Dysfunction of nucleus accumbens-1 activates cellular senescence and inhibits tumor cell proliferation and oncogenesis
Journal article   Open access   Peer reviewed

Dysfunction of nucleus accumbens-1 activates cellular senescence and inhibits tumor cell proliferation and oncogenesis

Yi Zhang, Yan Cheng, Xingcong Ren, Tsukasa Hori, Kathryn J Huber-Keener, Li Zhang, Kai Lee Yap, David Liu, Lisa Shantz, Zheng-Hong Qin, …
Cancer research (Chicago, Ill.), Vol.72(16), pp.4262-4275
08/15/2012
DOI: 10.1158/0008-5472.CAN-12-0139
PMCID: PMC3614094
PMID: 22665267
url
https://doi.org/10.1158/0008-5472.CAN-12-0139View
Published (Version of record) Open Access

Abstract

Nucleus accumbens-1 (NAC1), a nuclear factor belonging to the BTB/POZ gene family, has emerging roles in cancer. We report here that NAC1 acts as a negative regulator of cellular senescence in transformed and nontransformed cells, and dysfunction of NAC1 induces senescence and inhibits its oncogenic potential. We show that NAC1 deficiency markedly activates senescence and inhibits proliferation in tumor cells treated with sublethal doses of γ-irradiation. In mouse embryonic fibroblasts from NAC1 knockout mice, following infection with a Ras virus, NAC1-/- cells undergo significantly more senescence and are either nontransformed or less transformed in vitro and less tumorigenic in vivo when compared with NAC1+/+ cells. Furthermore, we show that the NAC1-caused senescence blunting is mediated by ΔNp63, which exerts its effect on senescence through p21, and that NAC1 activates transcription of ΔNp63 under stressful conditions. Our results not only reveal a previously unrecognized function of NAC1, the molecular pathway involved and its impact on pathogenesis of tumor initiation and development, but also identify a novel senescence regulator that may be exploited as a potential target for cancer prevention and treatment.
Transfection RNA, Small Interfering - genetics Humans Ovarian Neoplasms - pathology Cell Growth Processes - physiology Uterine Cervical Neoplasms - pathology Neoplasm Proteins - metabolism Ovarian Neoplasms - genetics Repressor Proteins - deficiency Uterine Cervical Neoplasms - metabolism Cell Transformation, Neoplastic - genetics Female Ovarian Neoplasms - metabolism Neoplasm Proteins - genetics Repressor Proteins - metabolism Proto-Oncogene Proteins p21(ras) - metabolism Tumor Suppressor Proteins - metabolism Tumor Suppressor Protein p53 - metabolism Cellular Senescence - physiology Repressor Proteins - genetics Uterine Cervical Neoplasms - genetics Cell Transformation, Neoplastic - metabolism Transcription Factors - metabolism Animals Mice, Nude Mice Neoplasm Proteins - deficiency HeLa Cells Cell Transformation, Neoplastic - pathology RNA, Small Interfering - administration & dosage

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