Inhibition of Breast Tumor Cell Growth by Ectopic Expression of p16/INK4A Via Combined Effects of Cell Cycle Arrest, Senescence and Apoptotic Induction, and Angiogenesis Inhibition
文献类型：期刊论文
| 作者 | Lu, Yi2,3,4; Zhang, Xiongwen1,3; Zhang, Jun2,4 |
| 刊名 | JOURNAL OF CANCER
 |
| 出版日期 | 2012 |
| 卷号 | 3页码:333-344 |
| 关键词 | adenovirus angiogenesis apoptosis breast cancer gene therapy p16 senescence |
| ISSN号 | 1837-9664 |
| DOI | 10.7150/jca.4046 |
| 文献子类 | Article |
| 英文摘要 | p16-mediated inhibition of cancer cell proliferation and tumor suppression have been studied before,; the common consensus is that p16's cell-cycle arrest function plays a primary role in these actions, with some additional apoptotic induction by p16. However, other effects of p16 that may potentially contribute to p16-mediated anti-tumor ability have not been well studied. The emerging data including ours indicated that p16 contributes its anti-cancer ability by inducing tumor cells to senescence. Moreover, we showed that p16 inhibits breast cancer cell growth by inhibiting the VEGF signaling pathway and angiogenesis. In this study, we used adenoviral-mediated p16 expression (AdRSVp16) and breast cancer cell line MDA-MB-231 as the model to simultaneously analyze all these p16's anti-tumor functions. We demonstrated that adenoviral-mediated p16 expression exhibited multiple anti-tumor functions by simultaneously suppressing in vitro growth and in vivo angiogenesis of breast cancer cells, blocking cell division, as well as inducing senescence and apoptosis. The in vivo study implies that p16's effect on anti-angiogenesis may play a more significant role than its anti-cell proliferation in the overall suppression of tumor growth. These results suggest, for the first time, that AdRSVp16-mediated tumor suppression results from a combination of p16's multiple anti-tumor functions including p16's well-known anti-proliferation/cell division function, apoptotic and senescence induction function, and its lesser-known/under-investigated anti-angiogenesis function. These combined results strongly indicate that p16 gene therapy has a multi-module platform with different anti-tumor functions; therefore, this study justifies and promotes the viral-mediated p16 gene therapy as a promising and powerful treatment approach for cancer patients due to p16's multiple anti-tumor functions. |
| WOS关键词 | SUPPRESSES PROSTATE-CANCER ; RECOMBINANT ADENOVIRUS ; HOMOZYGOUS DELETIONS ; GENE-THERAPY ; GLIOMA-CELLS ; P15 MTS2 ; CARCINOMA ; METASTASIS ; P16(INK4A) ; MUTATIONS |
| 资助项目 | NIH[DK65962] ; NIH[CA107162] |
| WOS研究方向 | Oncology |
| 语种 | 英语 |
| WOS记录号 | WOS:000318299800043 |
| 出版者 | IVYSPRING INT PUBL |
| 源URL | [http://119.78.100.183/handle/2S10ELR8/278226]  |
| 专题 | 中国科学院上海药物研究所 |
| 通讯作者 | Lu, Yi |
| 作者单位 | 1.Shanghai Inst Mat Med, Div Anticanc Pharmacol, Shanghai, Peoples R China 2.Univ Tennessee, Ctr Hlth Sci, Dept Pathol, Memphis, TN 38163 USA; 3.Univ Tennessee, Ctr Hlth Sci, Dept Urol, Memphis, TN 38163 USA; 4.Univ Tennessee, Ctr Hlth Sci, Dept Med, Memphis, TN 38163 USA; |
| 推荐引用方式 GB/T 7714 | Lu, Yi,Zhang, Xiongwen,Zhang, Jun. Inhibition of Breast Tumor Cell Growth by Ectopic Expression of p16/INK4A Via Combined Effects of Cell Cycle Arrest, Senescence and Apoptotic Induction, and Angiogenesis Inhibition[J]. JOURNAL OF CANCER,2012,3:333-344. |
| APA | Lu, Yi,Zhang, Xiongwen,&Zhang, Jun.(2012).Inhibition of Breast Tumor Cell Growth by Ectopic Expression of p16/INK4A Via Combined Effects of Cell Cycle Arrest, Senescence and Apoptotic Induction, and Angiogenesis Inhibition.JOURNAL OF CANCER,3,333-344. |
| MLA | Lu, Yi,et al."Inhibition of Breast Tumor Cell Growth by Ectopic Expression of p16/INK4A Via Combined Effects of Cell Cycle Arrest, Senescence and Apoptotic Induction, and Angiogenesis Inhibition".JOURNAL OF CANCER 3(2012):333-344. |
入库方式： OAI收割
来源：上海药物研究所
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