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| Content Provider | PubMed Central |
|---|---|
| Author | Sinha, Vidya C. Qin, Lan Li, Yi |
| Abstract | In response to oncogene activation and oncogene-induced aberrant proliferation, mammalian cells activate apoptosis and senescence, usually via the p53-ARF tumor suppressor pathway. Apoptosis is a known barrier to cancer and is usually down-regulated prior to full malignancy, but senescence as an anticancer barrier is controversial due to its presence in the tumor environment. In addition, senescence may aid cancer progression via releasing senescence-associated factors that instigate neighboring tumor cells. Here, it is demonstrated that apoptosis unexpectedly remains robust in ErbB2 (ERBB2/HER2)-initiated mammary early lesions arising in adult mice null for either p53 or ARF. These early lesions, however, down-regulate senescence significantly. This diminished senescence response is associated with accelerated progression to cancer in ARF-null mice compared to ARF-wild-type mice. Thus, the ARF-p53 pathway is dispensable for the apoptosis anticancer barrier in the initiation of ErbB2 breast cancer, the apoptosis barrier alone cannot halt mammary tumorigenesis, and that senescence is a key barrier against carcinogenesis. |
| Related Links | http://dx.doi.org/10.1158/1541-7786.mcr-14-0481-t |
| Ending Page | 238 |
| Page Count | 8 |
| Starting Page | 231 |
| File Format | |
| ISSN | 15417786 |
| e-ISSN | 15573125 |
| Journal | Molecular cancer research : MCR |
| Issue Number | 2 |
| Volume Number | 13 |
| Language | English |
| Publisher Date | 2015-02-01 |
| Access Restriction | Open |
| Subject Keyword | Cancer Research Oncology Molecular Biology Research in Higher Education |
| Content Type | Text |
| Resource Type | Article |
| Subject | Molecular Biology Cancer Research Oncology |
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