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[PRLZ过表达对前列腺癌LNCaP细胞体外侵袭的影响]

[Impact of PrLZ overexpression on invasion of prostate cancer LNCaP cells in vitro].

作者信息

Zhang Dong, Li Lei, Zhang Lin-Lin, Xue Yan, Wang Xin-Yang, He Da-Lin

机构信息

Department of Urology, The First Affiliated Hospital, Xi'an Jiaotong University, Xi'an, Shaanxi, China.

出版信息

Ai Zheng. 2009 May;28(5):483-6.

PMID:19624875
Abstract

BACKGROUND AND OBJECTIVE

Prostate leucine zipper (PrLZ), a novel gene, is highly associated with the malignant progression of prostate cancer. We previously found that PrLZ overexpression can enhance the survival of prostate cancer LNCaP cells in vitro. This study was to investigate the impact of PrLZ on the invasion of LNCaP cells and its possible mechanism.

METHODS

PrLZ was transfected into LNCaP cells. LNCaP/PrLZ cells with high expression of PrLZ were screened with G418. The migration and invasion of LNCaP and LNCaP/PrLZ cells were detected by Transwell assay. The level and activity of matrix metalloproteinase-2 (MMP-2) was determined by Western blot and Zymography, respectively.

RESULTS

Migration cell count of LNCaP and LNCaP/PrLZ cells were 64.8+/-8.7 and 69.3+/-7.6, respectively (P>0.05), whereas invasive cell count of LNCaP and LNCaP/PrLZ cells were 70.7+/-2.8 and 190.5+/-9.3, respectively (P<0.001). Both the expression and activity of MMP-2 in LNCaP/PrLZ cells were enhanced.

CONCLUSION

PrLZ may be involved in the invasion of prostate cancer.

摘要

背景与目的

前列腺亮氨酸拉链(PrLZ)是一种新基因,与前列腺癌的恶性进展高度相关。我们之前发现PrLZ过表达可增强前列腺癌LNCaP细胞在体外的存活率。本研究旨在探讨PrLZ对LNCaP细胞侵袭的影响及其可能机制。

方法

将PrLZ转染至LNCaP细胞。用G418筛选出PrLZ高表达的LNCaP/PrLZ细胞。采用Transwell实验检测LNCaP和LNCaP/PrLZ细胞的迁移和侵袭能力。分别通过蛋白质免疫印迹法和酶谱法测定基质金属蛋白酶-2(MMP-2)的水平和活性。

结果

LNCaP和LNCaP/PrLZ细胞的迁移细胞数分别为64.8±8.7和69.3±7.6(P>0.05),而LNCaP和LNCaP/PrLZ细胞的侵袭细胞数分别为70.7±2.8和190.5±9.3(P<0.001)。LNCaP/PrLZ细胞中MMP-2的表达和活性均增强。

结论

PrLZ可能参与前列腺癌的侵袭过程。

相似文献

1
[Impact of PrLZ overexpression on invasion of prostate cancer LNCaP cells in vitro].[PRLZ过表达对前列腺癌LNCaP细胞体外侵袭的影响]
Ai Zheng. 2009 May;28(5):483-6.
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PrLZ expression is associated with the progression of prostate cancer LNCaP cells.PrLZ表达与前列腺癌LNCaP细胞的进展相关。
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Loss of miR-449a-caused PrLZ overexpression promotes prostate cancer metastasis.miR-449a 缺失导致 PrLZ 过表达促进前列腺癌转移。
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PCPH/ENTPD5 expression enhances the invasiveness of human prostate cancer cells by a protein kinase C delta-dependent mechanism.PCPH/ENTPD5表达通过蛋白激酶Cδ依赖性机制增强人前列腺癌细胞的侵袭性。
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引用本文的文献

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PrLZ protects prostate cancer cells from apoptosis induced by androgen deprivation via the activation of Stat3/Bcl-2 pathway.PrLZ 通过激活 Stat3/Bcl-2 通路保护前列腺癌细胞免受雄激素剥夺诱导的细胞凋亡。
Cancer Res. 2011 Mar 15;71(6):2193-202. doi: 10.1158/0008-5472.CAN-10-1791. Epub 2011 Mar 8.