多效蛋白（PTN）是一種肝素結(jié)合生長(zhǎng)因子，具有促進(jìn)腫瘤生長(zhǎng),、血管生成和轉(zhuǎn)移等多種生物學(xué)功能,。PTN似乎在前列腺癌細(xì)胞生長(zhǎng)以及調(diào)控能影響前列腺癌細(xì)胞功能的其他刺激因子中有著特別的作用。然而,，所有的研究迄今為止都是在體外進(jìn)行的,，基本上就是使用了不同類型的人前列腺癌細(xì)胞株來(lái)開展研究。
近日發(fā)表在Cancer Sci的一項(xiàng)研究論文著重研究了體內(nèi)的內(nèi)源性PTN對(duì)人前列腺癌細(xì)胞生長(zhǎng)的作用,。為此,，科研人員將人前列腺癌PC-3細(xì)胞穩(wěn)定轉(zhuǎn)染有反義PTN序列的質(zhì)粒載體，目的是為了抑制PC-3細(xì)胞株的PTN表達(dá),。
在體外測(cè)定PC-3的遷移,、凋亡及對(duì)成骨細(xì)胞的黏附能力。皮下注入雄性NOD / SCID小鼠PC-3細(xì)胞,，檢測(cè)腫瘤的生長(zhǎng),、老鼠存活率、血管新生,、細(xì)胞凋亡和轉(zhuǎn)移的數(shù)量,。
體外實(shí)驗(yàn)數(shù)據(jù)顯示PTN的缺失導(dǎo)致PC-3細(xì)胞的遷移能力下降，同時(shí)PC-3細(xì)胞凋亡增加,，與成骨細(xì)胞的粘附能力降低,。在前列腺癌NOD/ SCID小鼠移植瘤中，PTN的缺失顯著抑制腫瘤的生長(zhǎng)和血管生成,，癌細(xì)胞凋亡增加,。
此外，體內(nèi)研究證實(shí)PTN的缺失導(dǎo)致腫瘤細(xì)胞的轉(zhuǎn)移降低,?？傊芯繑?shù)據(jù)表明在體內(nèi)PTN與人前列腺癌細(xì)胞的生長(zhǎng)密切相關(guān)，可作為前列腺癌新的治療靶標(biāo),。（生物谷：Bioon.com）
doi:10.1111/j.1349-7006.2012.02383.x
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Implication of pleiotrophin in human PC3 prostate cancer cell growth in vivo
Sotiria Tsirmoula1, Kostas Dimas2,3, Maria Hatziapostolou1, Margarita Lamprou1, Panagiota Ravazoula4, Evangelia Papadimitriou1,*
Pleiotrophin (PTN) is a heparin-binding growth factor with diverse functions related to tumor growth, angiogenesis and metastasis. PTN seems to have a significant role in prostate cancer cell growth and to mediate the stimulatory actions of other factors that affect prostate cancer cell functions. However, all studies performed up to date are in vitro, using different types of human prostate cancer cell lines. The aim of the present work was to study the role of endogenous PTN in human prostate cancer growth in vivo. For this purpose, human prostate cancer PC3 cells were stably transfected with a plasmid vector, bearing the antisense PTN sequence, in order to inhibit PTN expression (AS-PC3). Migration, apoptosis and adhesion on osteoblastic cells were measured in vitro. In vivo, PC3 cells were subcutaneously injected into male NOD/SCID mice, and tumor growth, survival rates, angiogenesis, apoptosis and the number of metastasis were estimated. PTN depletion resulted in a decreased migration capability of AS-PC3 cells compared with the corresponding mock-transfected or the non transfected PC3 cells, increased apoptosis and decreased adhesiveness to osteoblastic cells in vitro. In prostate cancer NOD/SCID mouse xenografts, PTN depletion significantly suppressed tumor growth and angiogenesis and induced apoptosis of cancer cells. In addition, PTN depletion decreased the number of metastases, providing a survival benefit for the animals bearing AS-PC3 xenografts. Our data suggest that PTN is implicated in human prostate cancer growth in vivo and may be considered as a potential target for the development of new therapeutic approaches for prostate cancer.
