Lentiviral Vector Mediated Claudin1 Silencing Inhibits Epithelial to Mesenchymal Transition in Breast Cancer Cells
| Autor: | Yanan Zou, Xianqi Zhao, Junming Yue, Qingqing Gu, Lawrence M. Pfeffer, Guannan Zhao, Horace Gray |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2015 |
| Předmět: |
Epithelial-Mesenchymal Transition
Cell Survival Genetic Vectors lcsh:QR1-502 Antineoplastic Agents Breast Neoplasms Biology Models Biological Article lcsh:Microbiology Metastasis Viral vector Small hairpin RNA Transformation Genetic Breast cancer breast cancer Cell Movement RNA interference Cell Line Tumor Virology Claudin-1 medicine Humans Gene silencing Gene Silencing Epithelial–mesenchymal transition RNA Small Interfering CLDN1 epithelial to mesenchymal transition Cell Proliferation Cell growth Lentivirus Epithelial Cells medicine.disease Infectious Diseases Cancer research Female RNA Interference |
| Zdroj: | Viruses Volume 7 Issue 6 Pages 2965-2979 Viruses, Vol 7, Iss 6, Pp 2965-2979 (2015) Viruses; Volume 7; Issue 6; Pages: 2965-2979 |
| ISSN: | 1999-4915 |
| DOI: | 10.3390/v7062755 |
| Popis: | Breast cancer has a high incidence and mortality rate worldwide. Several viral vectors including lentiviral, adenoviral and adeno-associated viral vectors have been used in gene therapy for various forms of human cancer, and have shown promising effects in controlling tumor development. Claudin1 (CLDN1) is a member of the tetraspan transmembrane protein family that plays a major role in tight junctions and is associated with tumor metastasis. However, the role of CLDN1 in breast cancer is largely unexplored. In this study, we tested the therapeutic potential of silencing CLDN1 expression in two breast cancer (MDA-MB-231 and MCF7) cell lines using lentiviral vector mediated RNA interference. We found that a CLDN1 short hairpin (shRNA) construct efficiently silenced CLDN1 expression in both breast cancer cell lines, and CLDN1 knockdown resulted in reduced cell proliferation, survival, migration and invasion. Furthermore, silencing CLDN1 inhibited epithelial to mesenchymal transition (EMT) by upregulating the epithelial cell marker, E-cadherin, and downregulating mesenchymal markers, smooth muscle cell alpha-actin (SMA) and Snai2. Our data demonstrated that lentiviral vector mediated CLDN1 RNA interference has great potential in breast cancer gene therapy by inhibiting EMT and controlling tumor cell growth. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|