Tumor suppressor dual-specificity phosphatase 6 (DUSP6) impairs cell invasion and epithelial-mesenchymal transition (EMT)-associated phenotype

2011 ◽  
Vol 130 (1) ◽  
pp. 83-95 ◽  
Author(s):  
Victor Chun Lam Wong ◽  
Han Chen ◽  
Josephine Mun Yee Ko ◽  
Kwok Wah Chan ◽  
Yuen Piu Chan ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Cell Invasion ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Dual Specificity Phosphatase ◽  
Dual Specificity

scholarly journals Exo70 Isoform Switching upon Epithelial-Mesenchymal Transition Mediates Cancer Cell Invasion

2013 ◽  
Vol 27 (5) ◽  
pp. 560-573 ◽  
Author(s):  
Hezhe Lu ◽  
Jianglan Liu ◽  
Shujing Liu ◽  
Jingwen Zeng ◽  
Deqiang Ding ◽  
...  
Keyword(s):  
Cancer Cell ◽  
Cell Invasion ◽  
Epithelial Mesenchymal Transition ◽  
Cancer Cell Invasion ◽  
Mesenchymal Transition ◽  
Isoform Switching

scholarly journals LRIG1 acts as a critical regulator of melanoma cell invasion, migration, and vasculogenic mimicry upon hypoxia by regulating EGFR/ERK-triggered epithelial–mesenchymal transition

2019 ◽  
Vol 39 (1) ◽  
Author(s):  
Wei Li ◽  
Yubo Zhou
Keyword(s):  
Melanoma Cell ◽  
Cell Invasion ◽  
Cancer Metastasis ◽  
Epithelial Mesenchymal Transition ◽  
Vasculogenic Mimicry ◽  
Growth Factor Receptor ◽  
Inhibition Mechanism ◽  
Mechanism Analysis ◽  
Mesenchymal Transition ◽  
Hypoxia Exposure

AbstractIntratumoral hypoxia is a well-known feature of solid cancers and constitutes a major contributor to cancer metastasis and poor outcomes including melanoma. Leucine-rich repeats and Ig-like domains 1 (LRIG1) participate in the aggressive progression of several tumors, where its expression is frequently decreased. In the present study, hypoxia exposure aggravated melanoma cell invasion, migration, vasculogenic mimicry (VM), and epithelial–mesenchymal transition (EMT). During this process, LRIG1 expression was also decreased. Importantly, overexpression of LRIG1 notably counteracted hypoxia-induced invasion, migration, and VM, which was further augmented after LRIG1 inhibition. Mechanism analysis corroborated that LRIG1 elevation muted hypoxia-induced EMT by suppressing E-cadherin expression and increasing N-cadherin expression. Conversely, cessation of LRIG1 further potentiated hypoxia-triggered EMT. Additionally, hypoxia stimulation activated the epidermal growth factor receptor (EGFR)/ERK pathway, which was dampened by LRIG1 up-regulation but further activated by LRIG1 inhibition. More important, blocking this pathway with its antagonist erlotinib abrogated LRIG1 suppression-induced EMT, and subsequently cell invasion, migration, and VM of melanoma cells under hypoxia. Together, these findings suggest that LRIG1 overexpression can antagonize hypoxia-evoked aggressive metastatic phenotype by suppressing cell invasion, migration, and VM via regulating EGFR/ERK-mediated EMT process. Therefore, these findings may provide a promising target for melanoma therapy.

scholarly journals RUNX1 suppresses breast cancer stemness and tumor growth

2018 ◽  
Author(s):  
Deli Hong ◽  
Andrew J. Fritz ◽  
Kristiaan H. Finstad ◽  
Mark P. Fitzgerald ◽  
Adam L. Viens ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Stem Cell ◽  
Tumor Suppressor ◽  
Cancer Stem Cell ◽  
Tumor Growth ◽  
Epithelial Mesenchymal Transition ◽  
Ectopic Expression ◽  
Cell Activity ◽  
Mesenchymal Transition

SummaryRecent studies have revealed that mutations in the transcription factor Runx1 are prevalent in breast tumors. Yet, how loss of Runx1 contributes to breast cancer (BCa) remains unresolved. We demonstrate for the first time that Runx1 represses the breast cancer stem cell (BCSC) phenotype and consequently, functions as a tumor suppressor in breast cancer. Runx1 ectopic expression in MCF10AT1 and MCF10CA1a BCa cells reduces (60%) migration, invasion and in vivo tumor growth in mouse mammary fat pad (P<0.05). Runx1 is decreased in BCSCs, and overexpression of Runx1 suppresses tumorsphere formation and reduces the BCSC population. Furthermore, Runx1 inhibits Zeb1 expression, while Runx1 depletion activates Zeb1 and the epithelial-mesenchymal transition. Mechanistically Runx1 functions as a tumor suppressor in breast cancer through repression of cancer stem cell activity. This key regulation of BCSCs by Runx1 may be shared in other epithelial carcinomas, highlighting the importance of Runx1 in solid tumors.

scholarly journals MicroRNA-200b suppresses cell invasion and metastasis by inhibiting the epithelial-mesenchymal transition in cervical carcinoma

2016 ◽  
Vol 13 (4) ◽  
pp. 3155-3160 ◽  
Author(s):  
YAN-XIANG CHENG ◽  
QI-FAN ZHANG ◽  
LI HONG ◽  
FENG PAN ◽  
JIN-LING HUANG ◽  
...  
Keyword(s):  
Cervical Carcinoma ◽  
Cell Invasion ◽  
Epithelial Mesenchymal Transition ◽  
Invasion And Metastasis ◽  
Mesenchymal Transition
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