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前列腺癌发生过程中的衰老途径。

The senescence pathway in prostatic carcinogenesis.

机构信息

Discipline of Pathology and Cancer Biology Research Laboratory, Molecular Medicine Research Group, School of Medicine, University of Western Sydney, Australia.

出版信息

Pathology. 2010;42(6):507-11. doi: 10.3109/00313025.2010.508791.

DOI:10.3109/00313025.2010.508791
PMID:20854067
Abstract

Prostate cancer is a disease of the old and with increasing life expectancy, its incidence will continue to increase in the future. Control of prostate cancer has involved androgen ablation as a routine form of therapy. However, after an initial response, therapy-resistant clones can appear and result in cancer progression and metastasis with high mortality. The precise mechanisms for the development of androgen resistance are yet uncertain. It appears to be multi-factorial and relates not only to newly acquired genomic capabilities of the cancer cells but also to their interaction with their microenvironment. Overcoming cellular senescence is essential for oncogenesis. Although it seems to be a protective response for normal cells to avoid malignant transformation, senescence can on the other hand promote tumour progression. Interaction of senescent cancer cells with their microenvironment may be the key link to survival or regression of neoplastic cells. Hence, there is speculation that senescence may be a useful new target for therapy in the future. We review the role of senescence in prostate cancer and the effect of tumour microenvironment on androgen resistance.

摘要

前列腺癌是一种老年病,随着预期寿命的延长,其发病率在未来将继续上升。前列腺癌的治疗一直包括雄激素剥夺治疗作为常规治疗方法。然而,在初始反应后,可能会出现耐药克隆,导致癌症进展和转移,死亡率很高。雄激素耐药的确切机制尚不确定。它似乎是多因素的,不仅与癌细胞新获得的基因组能力有关,还与其微环境相互作用有关。克服细胞衰老对于致癌作用至关重要。虽然对于正常细胞来说,衰老似乎是一种避免恶性转化的保护反应,但衰老另一方面也可以促进肿瘤进展。衰老的癌细胞与其微环境的相互作用可能是肿瘤细胞存活或消退的关键环节。因此,有人推测衰老可能是未来治疗的一个有用的新靶点。我们回顾了衰老在前列腺癌中的作用以及肿瘤微环境对雄激素耐药性的影响。

相似文献

1
The senescence pathway in prostatic carcinogenesis.前列腺癌发生过程中的衰老途径。
Pathology. 2010;42(6):507-11. doi: 10.3109/00313025.2010.508791.
2
Function of JunB in transient amplifying cell senescence and progression of human prostate cancer.JunB在人前列腺癌瞬时扩增细胞衰老和进展中的作用
Clin Cancer Res. 2008 Jul 15;14(14):4408-16. doi: 10.1158/1078-0432.CCR-07-4120.
3
Molecular insights into prostate cancer progression: the missing link of tumor microenvironment.前列腺癌进展的分子见解:肿瘤微环境的缺失环节
J Urol. 2005 Jan;173(1):10-20. doi: 10.1097/01.ju.0000141582.15218.10.
4
The gene expression program of prostate fibroblast senescence modulates neoplastic epithelial cell proliferation through paracrine mechanisms.前列腺成纤维细胞衰老的基因表达程序通过旁分泌机制调节肿瘤上皮细胞增殖。
Cancer Res. 2006 Jan 15;66(2):794-802. doi: 10.1158/0008-5472.CAN-05-1716.
5
[Recent findings on the pathogenesis and therapy of prostatic cancer].[前列腺癌发病机制与治疗的最新研究成果]
Urologe A. 1988 Mar;27(2):105-10.
6
Differentiation pathways and histogenetic aspects of normal and abnormal prostatic growth: a stem cell model.正常和异常前列腺生长的分化途径及组织发生学方面:一种干细胞模型
Prostate. 1996 Feb;28(2):98-106. doi: 10.1002/(SICI)1097-0045(199602)28:2<98::AID-PROS4>3.0.CO;2-J.
7
Malignant transformation of human prostatic epithelium is associated with the loss of androgen receptor immunoreactivity in the surrounding stroma.人类前列腺上皮的恶性转化与周围基质中雄激素受体免疫反应性的丧失有关。
Clin Cancer Res. 1999 Mar;5(3):569-76.
8
Characterization of epithelial senescence by serial analysis of gene expression: identification of genes potentially involved in prostate cancer.通过基因表达序列分析对上皮细胞衰老进行特征描述:鉴定可能与前列腺癌相关的基因。
Cancer Res. 2002 Nov 1;62(21):6255-62.
9
Cancer, aging and cellular senescence.癌症、衰老与细胞衰老
In Vivo. 2000 Jan-Feb;14(1):183-8.
10
Role of IFI 16, a member of the interferon-inducible p200-protein family, in prostate epithelial cellular senescence.干扰素诱导的p200蛋白家族成员IFI 16在前列腺上皮细胞衰老中的作用。
Oncogene. 2003 Jul 31;22(31):4831-40. doi: 10.1038/sj.onc.1206754.

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Ginsenoside Rg3 inhibits the senescence of prostate stromal cells through down-regulation of interleukin 8 expression.人参皂苷Rg3通过下调白细胞介素8的表达来抑制前列腺基质细胞的衰老。
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