scholarly journals Down-regulation of MT1-MMP expression suppresses tumor cell invasion in metastatic human SW626 ovarian cancer cells

2006 ◽  
Author(s):  
Mingfu Wu ◽  
Gang Xu ◽  
Ling Xi ◽  
Junchen Wei ◽  
Anping Song ◽  
...  
Oncotarget ◽  
2016 ◽  
Vol 7 (49) ◽  
pp. 81645-81660 ◽  
Author(s):  
Jung-Chien Cheng ◽  
Hsun-Ming Chang ◽  
Siyuan Xiong ◽  
Wai-Kin So ◽  
Peter C. K. Leung

2012 ◽  
Vol 421 (2) ◽  
pp. 190-196 ◽  
Author(s):  
Hai Yang Yu ◽  
Kyoung-Sook Kim ◽  
Hyung-In Moon ◽  
Kyung-Mi Kim ◽  
Young-Choon Lee ◽  
...  

Tumor Biology ◽  
2016 ◽  
Vol 37 (7) ◽  
pp. 9197-9207 ◽  
Author(s):  
Wai-Kin So ◽  
Jung-Chien Cheng ◽  
Yingtao Liu ◽  
Congjian Xu ◽  
Jianfang Zhao ◽  
...  

Cancers ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 2745
Author(s):  
Miran Jeong ◽  
Yi-Yue Wang ◽  
Ju-Yeon Choi ◽  
Myong-Cheol Lim ◽  
Jung-Hye Choi

In the tumor microenvironment, macrophages have been suggested to be stimulated by tumor cells, becoming tumor-associated macrophages that promote cancer development and progression. We examined the effect of these macrophages on human ovarian cancer cell invasion and found that conditioned medium of macrophages stimulated by ovarian cancer cells (OC-MQs) significantly increased cell invasion. CC chemokine ligand 7 (CCL7) expression and production were significantly higher in OC-MQs than in the control macrophages. Peritoneal macrophages from patients with ovarian cancer showed higher CCL7 expression levels than those from healthy controls. Inhibition of CCL7 using siRNA and neutralizing antibodies reduced the OC-MQ-CM-induced ovarian cancer cell invasion. CC chemokine receptor 3 (CCR3) was highly expressed in human ovarian cancer cells, and a specific inhibitor of this receptor reduced the OC-MQ-CM-induced invasion. Specific signaling and transcription factors were associated with enhanced CCL7 expression in OC-MQs. CCL7-induced invasion required the expression of matrix metalloproteinase 9 via activation of extracellular signal-related kinase signaling in human ovarian cancer cells. These data suggest that tumor-associated macrophages can affect human ovarian cancer metastasis via the CCL7/CCR3 axis.


2021 ◽  
Vol 17 (1) ◽  
pp. 127-134
Author(s):  
Min Wei ◽  
Hongjuan Jin ◽  
ShuLi Yang ◽  
Zhuo Li ◽  
Xinlei Wang ◽  
...  

IntroductionOvarian cancer is the most frequent cause of gynecological cancer related mortality in woman. This study was designed to investigate the role and therapeutic potential of miRNA-101 in ovarian cancer.Material and methodsExpression analysis was carried out by real-time quantitative polymerase chain reaction. Transfections were performed with the help of Lipofectamine 2000 reagent. AO/EB and annexin V/PI staining was used to detect apoptosis and flow cytometry was used for cell cycle analysis. Western blotting was employed for cell cycle analysis.ResultsIt was found that miRNA-101 was significantly down-regulated in ovarian cancer cells. The over-expression of miRNA-101 causes a significant decrease in the viability of ovarian cancer cells via the initiation of apoptosis and sub-G1 arrest of OVACAR-3 cells. It was indicated that PTEN was the potential target of miRNA-101 in OVACAR-3 cells. There was 4.5-fold up-regulation of PTEN expression in ovarian cancer cell lines and the over-expression of miRNA-101 in OVACAR-3 cells resulted in the down-regulation of PTEN expression. The inhibition of PTEN in the OVACAR-3 cells arrested the proliferation of these cells. The over-expression of miRNA-101 causes significant down-regulation in PI3K and AKT expression of OVACAR-3 cells.ConclusionsIt can be concluded that miRNA-101 acts as a tumor suppressor which may be beneficial in the treatment of ovarian cancer.


2016 ◽  
Vol 311 (6) ◽  
pp. C1040-C1047 ◽  
Author(s):  
Chun-Min Lo ◽  
Jun-Chih Lo ◽  
Priscila Y. Sato ◽  
Tsz-Lun Yeung ◽  
Samuel C. Mok ◽  
...  

The conventional approach to assessing cancer invasion is primarily for end-point analysis, which does not provide temporal information on the invasion process or any information on the interactions between invading cells and the underlying adherent cells. To alleviate these limitations, the present study exploited electric cell-substrate impedance sensing (ECIS) to monitor the invasion of ovarian cancer cells (SKOV-3) through an adherent monolayer of human umbilical vein endothelial cells (HUVECs). Impedance was measured at 4 kHz of AC voltage or was measured as a function of AC frequency (25 Hz to 60 kHz). By measuring impedance at 4-kHz AC, we found that the invasion of SKOV-3 cells through the HUVEC monolayer was manifested as a rapid decrease in transendothelial electrical resistance in real time. The invasion was augmented in the presence of hepatocyte growth factor (HGF). The enhancing effect of HGF was attenuated by c-Met inhibitor (SU11274). By measuring the frequency-dependent impedance of SKOV-3 cells over time, we found that HGF-enhanced SKOV-3 cell invasion was accomplished with reduced junctional resistance ( Rb), increased average cell-substrate separation ( h), and increased micromotion. SU11274 attenuated the effects of HGF on Rb, h, and micromotion in the SKOV-3 monolayer. SU11274 also increased the barrier function of the HUVEC monolayer by increasing Rb and decreasing h. In conclusion, this study demonstrated an improved method for monitoring and studying the interactions between cancer cells and the underlying adherent cells during invasion in real time. Alterations in cellular biophysical properties ( Rb, h) associated with cancer transendothelial invasion were detected.


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