Increased levels of LAPTM4B, VEGF and survivin are correlated with tumor progression and poor prognosis in breast cancer patients

LAPTM4B、VEGF 和 survivin 水平升高与乳腺癌患者的肿瘤进展和不良预后相关

阅读:16
作者:Sha Li, Lu Wang, Yue Meng, Yanli Chang, Jianjun Xu, Qingyun Zhang

Conclusions

These findings suggest that LAPTM4B, VEGF, and nuclear survivin expression are significantly correlated in breast cancer, which may be predictive of prognosis as well as effective therapeutic targets for new anticancer therapies.

Methods

The expression of these three molecules in 110 stage I-III breast cancer patients with clinicopathological and follow-up data was detected via immunohistochemistry. Kaplan-Meier and Cox proportional hazard regression analyses were performed to assess the prognostic significance of these markers in breast cancer. Moreover, expression levels of these markers were evaluated in 5 breast cell lines via Western blot analysis.

Objective

This study explored the relationships among the expression of LAPTM4B, VEGF, and survivin and clinicopathological characteristics and prognosis in breast cancer patients.

Results

LAPTM4B, VEGF, and survivin were over-expressed in breast cancer specimens and highly expressed in MDA-MB-231 cells. VEGF and nuclear survivin expression was significantly correlated with LAPTM4B expression, and high levels of all three were associated with a tumor size >2cm, TNM stage II+III and lymph node metastasis, which had worse impacts on overall survival and progression-free survival in breast cancer patients. A multivariate Cox analysis identified LAPTM4B over-expression as an independent prognostic marker in breast cancer. Conclusions: These findings suggest that LAPTM4B, VEGF, and nuclear survivin expression are significantly correlated in breast cancer, which may be predictive of prognosis as well as effective therapeutic targets for new anticancer therapies.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。