scholarly journals Inhibition of CD147 gene expression via RNA interference reduces tumor cell invasion, tumorigenicity and increases chemosensitivity to cisplatin in laryngeal carcinoma Hep2 cells

2011 ◽  
Vol 25 (2) ◽  
Author(s):  
Wang
Keyword(s):  
Gene Expression ◽  
Rna Interference ◽  
Tumor Cell ◽  
Cell Invasion ◽  
Laryngeal Carcinoma ◽  
Tumor Cell Invasion

scholarly journals Inhibition of cathepsin B and MMP-9 gene expression in glioblastoma cell line via RNA interference reduces tumor cell invasion, tumor growth and angiogenesis

Oncogene ◽  
2004 ◽  
Vol 23 (27) ◽  
pp. 4681-4689 ◽  
Author(s):  
Sajani S Lakka ◽  
Christopher S Gondi ◽  
Niranjan Yanamandra ◽  
William C Olivero ◽  
Dzung H Dinh ◽  
...  
Keyword(s):  
Gene Expression ◽  
Rna Interference ◽  
Tumor Growth ◽  
Tumor Cell ◽  
Cell Line ◽  
Cell Invasion ◽  
Cathepsin B ◽  
Tumor Cell Invasion ◽  
Glioblastoma Cell Line ◽  
Glioblastoma Cell

scholarly journals RNA Interference-directed Knockdown of Urokinase Plasminogen Activator and Urokinase Plasminogen Activator Receptor Inhibits Prostate Cancer Cell Invasion, Survival, and Tumorigenicity in Vivo

2005 ◽  
Vol 280 (43) ◽  
pp. 36529-36540 ◽  
Author(s):  
Sai MuraliKrishna Pulukuri ◽  
Christopher S. Gondi ◽  
Sajani S. Lakka ◽  
Aman Jutla ◽  
Norman Estes ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Rna Interference ◽  
Tumor Cell ◽  
Plasminogen Activator ◽  
Cancer Cell ◽  
Cell Invasion ◽  
Prostate Cancer Cell ◽  
Urokinase Plasminogen Activator ◽  
Tumor Cell Invasion ◽  
Upar Expression

The invasive ability of tumor cells plays a key role in prostate cancer metastasis and is a major cause of treatment failure. Urokinase plasminogen activator-(uPA) and its receptor (uPAR)-mediated signaling have been implicated in tumor cell invasion, survival, and metastasis in a variety of cancers. This study was undertaken to investigate the biological roles of uPA and uPAR in prostate cancer cell invasion and survival, and the potential of uPA and uPAR as targets for prostate cancer therapy. uPA and uPAR expression correlates with the metastatic potential of prostate cancer cells. Thus, therapies designed to inhibit uPA and uPAR expression would be beneficial. LNCaP, DU145, and PC3 are prostate cancer cell lines with low, moderate, and high metastatic potential, respectively, as demonstrated by their capacity to invade the extracellular matrix. In this study we utilized small hairpin RNAs (shRNAs), also referred to as small interfering RNAs, to target human uPA and uPAR. These small interfering RNA constructs significantly inhibited uPA and uPAR expression at both the mRNA and protein levels in the highly metastatic prostate cancer cell line PC3. Our data demonstrated that uPA-uPAR knockdown in PC3 cells resulted in a dramatic reduction of tumor cell invasion as indicated by a Matrigel invasion assay. Furthermore, simultaneous silencing of the genes for uPA and uPAR using a single plasmid construct expressing shRNAs for both uPA and uPAR significantly reduced cell viability and ultimately resulted in the induction of apoptotic cell death. RNA interference for uPA and uPAR also abrogated uPA-uPAR signaling to downstream target molecules such as ERK1/2 and Stat 3. In addition, our results demonstrated that intratumoral injection with the plasmid construct expressing shRNAs for uPA and uPAR almost completely inhibited established tumor growth and survival in an orthotopic mouse prostate cancer model. These findings uncovered evidence of a complex signaling network operating downstream of uPA-uPAR that actively advances tumor cell invasion, proliferation, and survival of prostate cancer cells. Thus, RNA interference-directed targeting of uPA and uPAR is a convenient and novel tool for studying the biological role of the uPA-uPAR system and raises the potential of its application for prostate cancer therapy.

scholarly journals Collagen-rich stroma in aggressive colon tumors induces mesenchymal gene expression and tumor cell invasion

Oncogene ◽  
2016 ◽  
Vol 35 (40) ◽  
pp. 5263-5271 ◽  
Author(s):  
T T Vellinga ◽  
S den Uil ◽  
I H B Rinkes ◽  
D Marvin ◽  
B Ponsioen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Tumor Cell ◽  
Cell Invasion ◽  
Tumor Cell Invasion ◽  
Colon Tumors

scholarly journals AP-1 Differentially Expressed Proteins Krp1 and Fibronectin Cooperatively Enhance Rho-ROCK-Independent Mesenchymal Invasion by Altering the Function, Localization, and Activity of Nondifferentially Expressed Proteins

2006 ◽  
Vol 26 (4) ◽  
pp. 1480-1495 ◽  
Author(s):  
Heather J. Spence ◽  
Lynn McGarry ◽  
Catherine S. Chew ◽  
Neil O. Carragher ◽  
Linda A. Scott-Carragher ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Tumor Cell ◽  
Cell Invasion ◽  
Essential Role ◽  
Differentially Expressed ◽  
Tumor Cell Invasion ◽  
Actin Binding ◽  
Fibroblast Cells ◽  
Differentially Expressed Proteins

ABSTRACT The transcription factor AP-1, which is composed of Fos and Jun family proteins, plays an essential role in tumor cell invasion by altering gene expression. We report here that Krp1, the AP-1 up-regulated protein that has a role in pseudopodial elongation in v-Fos-transformed rat fibroblast cells, forms a novel interaction with the nondifferentially expressed actin binding protein Lasp-1. Krp1 and Lasp-1 colocalize with actin at the tips of pseudopodia, and this localization is maintained by continued AP-1 mediated down-regulation of fibronectin that in turn suppresses integrin and Rho-ROCK signaling and allows pseudopodial protrusion and mesenchyme-like invasion. Mutation analysis of Lasp-1 demonstrates that its SH3 domain is necessary for pseudopodial extension and invasion. The results support the concept of an AP-1-regulated multigenic invasion program in which proteins encoded by differentially expressed genes direct the function, localization, and activity of proteins that are not differentially expressed to enhance the invasiveness of cells.

CUTL1–a modulator of tumor cell invasion and target of TGF-beta which is highly expressed in colon cancer

2004 ◽  
Vol 42 (08) ◽  
Author(s):  
P Michl ◽  
M Ei'Bahrawy ◽  
R Poulsom ◽  
A Ramjaun ◽  
J Downward
Keyword(s):  
Colon Cancer ◽  
Tumor Cell ◽  
Cell Invasion ◽  
Tumor Cell Invasion ◽  
Tgf Beta
Sign in / Sign up

Export Citation Format

Share Document