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CAV2通过表皮生长因子受体/磷脂酰肌醇-3激酶/蛋白激酶B信号通路促进肾细胞癌的生长。

CAV2 promotes the growth of renal cell carcinoma through the EGFR/PI3K/Akt pathway.

作者信息

Liu Fu, Shangli Zhi, Hu Zhili

机构信息

The First People's Hospital of Ziyang, Sichuan, People's Republic of China,

The Second Hospital Affiliated to Chongqing Medical University, Chongqing, People's Republic of China.

出版信息

Onco Targets Ther. 2018 Sep 25;11:6209-6216. doi: 10.2147/OTT.S172803. eCollection 2018.

DOI:10.2147/OTT.S172803
PMID:30288056
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6163017/
Abstract

BACKGROUND

Caveolin-2 (CAV2) is reported to have an important role in cancer. The following study investigated the expression and function of CAV2 in kidney cancer in vitro and in vivo.

MATERIALS AND METHODS

Real-time PCR, immunohistochemistry and Western blotting analysis were used to determine CAV2, epidermal growth factor receptor (EGFR), phosphatidylinositol 3-kinase (PI3K) and protein kinase B (Akt) in kidney cancer cell line OS-RC-2 and clinical specimens. The role of CAV2 in maintaining kidney cancer malignant phenotype was examined by wound healing assay, Matrigel invasion assays and mouse orthotopic xenograft model.

RESULTS

Higher expression of CAV2 was found in renal cell carcinoma tissue compared to normal tissue. Furthermore, increased expression of CAV2 was associated with cancer progression. Also, silencing of CAV2 inhibited the proliferation, migration and invasion, as well as the expression of EGFR, PI3K and p-Akt in OS-RC-2 cells in vitro, and OS-RC-2 xenograft growth in vivo.

CONCLUSION

Our results revealed that CAV2 promotes the growth of renal cell carcinoma through EGFR/PI3K/Akt pathway.

摘要

背景

据报道，小窝蛋白2（CAV2）在癌症中发挥重要作用。以下研究在体外和体内研究了CAV2在肾癌中的表达及功能。

材料与方法

采用实时聚合酶链反应、免疫组织化学及蛋白质印迹分析，检测肾癌细胞系OS-RC-2及临床标本中的CAV2、表皮生长因子受体（EGFR）、磷脂酰肌醇3激酶（PI3K）和蛋白激酶B（Akt）。通过伤口愈合试验、基质胶侵袭试验及小鼠原位异种移植模型，研究CAV2在维持肾癌恶性表型中的作用。

结果

与正常组织相比，肾细胞癌组织中CAV2表达更高。此外，CAV2表达增加与癌症进展相关。而且，在体外，CAV2沉默抑制了OS-RC-2细胞的增殖、迁移和侵袭，以及EGFR、PI3K和p-Akt的表达；在体内，CAV2沉默抑制了OS-RC-2异种移植瘤的生长。

结论

我们的结果表明，CAV2通过EGFR/PI3K/Akt途径促进肾细胞癌的生长。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/096a/6163017/88e7f3399dfb/ott-11-6209Fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/096a/6163017/17d63c6d316c/ott-11-6209Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/096a/6163017/f5dc7fd90f09/ott-11-6209Fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/096a/6163017/ec2b6856ff3a/ott-11-6209Fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/096a/6163017/c1376a234ddd/ott-11-6209Fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/096a/6163017/88e7f3399dfb/ott-11-6209Fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/096a/6163017/17d63c6d316c/ott-11-6209Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/096a/6163017/f5dc7fd90f09/ott-11-6209Fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/096a/6163017/ec2b6856ff3a/ott-11-6209Fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/096a/6163017/c1376a234ddd/ott-11-6209Fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/096a/6163017/88e7f3399dfb/ott-11-6209Fig5.jpg

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