RIOK2 is negatively regulated by miR‐4744 and promotes glioma cell migration/invasion through epithelial‐mesenchymal transition

Abstract LINC00599 has been suggested to be involved in physiological and pathological processes including carcinogenesis. However, the clinical and prognostic significance of LINC00599 in glioma patients and the effect of LINC00599 on glioma cell migration and invasion remain unknown. In our results, we first observe the expression of LINC00599 in 31 types of human cancers including tumor tissues and corresponding normal tissues at The Cancer Genome Atlas (TCGA) database, and found that LINC00599 expression levels were only reduced in lower grade glioma (LGG) tissues and glioblastoma multiforme (GBM) tissues compared with normal brain tissues. Moreover, we confirmed levels of LINC00599 expression were decreased in glioma tissues and cell lines compared with matched adjacent normal tissues and normal human astrocytes (NHAs), respectively. Meanwhile, we found that glioma tissues with WHO III-IV grade exhibited lower levels of LINC00599 expression than glioma tissues with I-II grade. The survival analysis at TCGA data showed low LINC00599 expression was associated with poor disease-free survival and overall survival in glioma patients. In vitro study suggested up-regulation of LINC00599 depressed glioma cell migration and invasion through regulating epithelial–mesenchymal transition (EMT) process. In conclusion, LINC00599 acts as a tumor-suppressing long non-coding RNA (lncRNA) in glioma.

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Exendin-4 inhibits glioma cell migration, invasion and epithelial-to-mesenchymal transition through GLP-1R/sirt3 pathway

Biomedicine & Pharmacotherapy ◽

10.1016/j.biopha.2018.07.092 ◽

2018 ◽

Vol 106 ◽

pp. 1364-1369 ◽

Cited By ~ 3

Author(s):

Zhi-Jun Nie ◽

Yin-Gang Zhang ◽

Yan-Hai Chang ◽

Quan-Yi Li ◽

Yue-Lin Zhang

Keyword(s):

Cell Migration ◽

Glioma Cell ◽

Epithelial To Mesenchymal Transition ◽

Mesenchymal Transition ◽

Glioma Cell Migration

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Visfatin facilitates gastric cancer malignancy by targeting snai1 via the NF-κB signaling

Human & Experimental Toxicology ◽

10.1177/09603271211006168 ◽

2021 ◽

pp. 096032712110061

Author(s):

D Cao ◽

L Chu ◽

Z Xu ◽

J Gong ◽

R Deng ◽

...

Keyword(s):

Gastric Cancer ◽

Cell Migration ◽

Western Blot ◽

Blot Analysis ◽

Western Blot Analysis ◽

Epithelial Mesenchymal Transition ◽

Migration And Invasion ◽

Mesenchymal Transition ◽

Cell Migration And Invasion ◽

Protein Levels

Background: Visfatin acts as an oncogenic factor in numerous tumors through a variety of cellular processes. Visfatin has been revealed to promote cell migration and invasion in gastric cancer (GC). Snai1 is a well-known regulator of EMT process in cancers. However, the relationship between visfatin and snai1 in GC remains unclear. The current study aimed to explore the role of visfatin in GC. Methods: The RT-qPCR and western blot analysis were used to measure RNA and protein levels, respectively. The cell migration and invasion were tested by Trans-well assays and western blot analysis. Results: Visfatin showed upregulation in GC cells. Additionally, Visfatin with increasing concentration facilitated epithelial-mesenchymal transition (EMT) process by increasing E-cadherin and reducing N-cadherin and Vimentin protein levels in GC cells. Moreover, endogenous overexpression and knockdown of visfatin promoted and inhibited migratory and invasive abilities of GC cells, respectively. Then, we found that snai1 protein level was positively regulated by visfatin in GC cells. In addition, visfatin activated the NF-κB signaling to modulate snai1 protein expression. Furthermore, the silencing of snai1 counteracted the promotive impact of visfatin on cell migration, invasion and EMT process in GC. Conclusion: Visfatin facilitates cell migration, invasion and EMT process by targeting snai1 via the NF-κB signaling, which provides a potential insight for the treatment of GC.

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Overexpression of heat shock protein 70 inhibits epithelial-mesenchymal transition and cell migration induced by transforming growth factor-β in A549 cells

Cell Stress and Chaperones ◽

10.1007/s12192-021-01196-3 ◽

2021 ◽

Vol 26 (3) ◽

pp. 505-513

Author(s):

Fengxian Shi ◽

Mingze Ma ◽

Ruonan Zhai ◽

Yanan Ren ◽

Ke Li ◽

...

Keyword(s):

Cell Migration ◽

Growth Factor ◽

Heat Shock ◽

Heat Shock Protein ◽

Heat Shock Protein 70 ◽

Transforming Growth Factor ◽

Epithelial Mesenchymal Transition ◽

A549 Cells ◽

Transforming Growth Factor Β ◽

Mesenchymal Transition

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Involvement of the ERK/HIF-1α/EMT Pathway in XCL1-Induced Migration of MDA-MB-231 and SK-BR-3 Breast Cancer Cells

International Journal of Molecular Sciences ◽

10.3390/ijms22010089 ◽

2020 ◽

Vol 22 (1) ◽

pp. 89

Author(s):

Ha Thi Thu Do ◽

Jungsook Cho

Keyword(s):

Breast Cancer ◽

Cell Migration ◽

Cancer Cells ◽

Cancer Progression ◽

Chemokine Receptor ◽

Intracellular Signaling ◽

Breast Cancer Cells ◽

Epithelial Mesenchymal Transition ◽

Mitogen Activated Protein Kinase ◽

Mesenchymal Transition

Chemokine–receptor interactions play multiple roles in cancer progression. It was reported that the overexpression of X-C motif chemokine receptor 1 (XCR1), a specific receptor for chemokine X-C motif chemokine ligand 1 (XCL1), stimulates the migration of MDA-MB-231 triple-negative breast cancer cells. However, the exact mechanisms of this process remain to be elucidated. Our study found that XCL1 treatment markedly enhanced MDA-MB-231 cell migration. Additionally, XCL1 treatment enhanced epithelial–mesenchymal transition (EMT) of MDA-MB-231 cells via E-cadherin downregulation and upregulation of N-cadherin and vimentin as well as increases in β-catenin nucleus translocation. Furthermore, XCL1 enhanced the expression of hypoxia-inducible factor-1α (HIF-1α) and phosphorylation of extracellular signal-regulated kinase (ERK) 1/2. Notably, the effects of XCL1 on cell migration and intracellular signaling were negated by knockdown of XCR1 using siRNA, confirming XCR1-mediated actions. Treating MDA-MB-231 cells with U0126, a specific mitogen-activated protein kinase kinase (MEK) 1/2 inhibitor, blocked XCL1-induced HIF-1α accumulation and cell migration. The effect of XCL1 on cell migration was also evaluated in ER-/HER2+ SK-BR-3 cells. XCL1 also promoted cell migration, EMT induction, HIF-1α accumulation, and ERK phosphorylation in SK-BR-3 cells. While XCL1 did not exhibit any significant impact on the matrix metalloproteinase (MMP)-2 and -9 expressions in MDA-MB-231 cells, it increased the expression of these enzymes in SK-BR-3 cells. Collectively, our results demonstrate that activation of the ERK/HIF-1α/EMT pathway is involved in the XCL1-induced migration of both MDA-MB-231 and SK-BR-3 breast cancer cells. Based on our findings, the XCL1–XCR1 interaction and its associated signaling molecules may serve as specific targets for the prevention of breast cancer cell migration and metastasis.

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Neural crest migration: interplay between chemorepellents, chemoattractants, contact inhibition, epithelial-mesenchymal transition, and collective cell migration

Wiley Interdisciplinary Reviews Developmental Biology ◽

10.1002/wdev.28 ◽

2012 ◽

Vol 1 (3) ◽

pp. 435-445 ◽

Cited By ~ 62

Author(s):

Eric Theveneau ◽

Roberto Mayor

Keyword(s):

Cell Migration ◽

Neural Crest ◽

Epithelial Mesenchymal Transition ◽

Contact Inhibition ◽

Collective Cell Migration ◽

Mesenchymal Transition ◽

Neural Crest Migration

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MicroRNA-520c inhibits glioma cell migration and invasion by the suppression of transforming growth factor-β receptor type 2

Oncology Reports ◽

10.3892/or.2017.5421 ◽

2017 ◽

Vol 37 (3) ◽

pp. 1691-1697 ◽

Cited By ~ 10

Author(s):

Shengli Hu ◽

Huibin Chen ◽

Yuqiang Zhang ◽

Chaojia Wang ◽

Kaijun Liu ◽

...

Keyword(s):

Cell Migration ◽

Growth Factor ◽

Glioma Cell ◽

Transforming Growth Factor ◽

Transforming Growth Factor Β ◽

Receptor Type ◽

Migration And Invasion ◽

Β Receptor ◽

Glioma Cell Migration

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Downregulation of PAK5 inhibits glioma cell migration and invasion potentially through the PAK5-Egr1-MMP2 signaling pathway

Brain Tumor Pathology ◽

10.1007/s10014-013-0161-1 ◽

2013 ◽

Vol 31 (4) ◽

pp. 234-241 ◽

Cited By ~ 26

Author(s):

Zheng-Xiang Han ◽

Xiao-Xia Wang ◽

Shang-Nuan Zhang ◽

Jin-Xia Wu ◽

He-ya Qian ◽

...

Keyword(s):

Cell Migration ◽

Signaling Pathway ◽

Glioma Cell ◽

Migration And Invasion ◽

Cell Migration And Invasion ◽

Glioma Cell Migration

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Fiber density and matrix stiffness modulate distinct cell migration modes in a 3D stroma mimetic composite hydrogel

10.1101/2021.02.27.433190 ◽

2021 ◽

Author(s):

Harrison L. Hiraki ◽

Daniel L. Matera ◽

William Y. Wang ◽

Alexander A. Zarouk ◽

Anna E. Argento ◽

...

Keyword(s):

Cell Migration ◽

Epithelial Mesenchymal Transition ◽

Cancer Therapeutics ◽

Therapy Resistance ◽

Metastatic Spread ◽

Tumor Escape ◽

Fiber Density ◽

Mesenchymal Transition ◽

Stromal Microenvironment ◽

Induced Apoptosis

ABSTRACTThe peritumoral stroma is a complex 3D tissue that provides cells with myriad biophysical and biochemical cues. Histologic observations suggest that during metastatic spread of carcinomas, these cues influence transformed epithelial cells, prompting a diversity of migration modes spanning single cell and multicellular phenotypes. Purported consequences of these variations in tumor escape strategies include differential metastatic capability and therapy resistance. Therefore, understanding how cues from the peritumoral stromal microenvironment regulate migration mode phenotypes has prognostic and therapeutic value. Here, we utilize a synthetic stromal mimetic in which matrix fiber density and bulk hydrogel stiffness can be orthogonally tuned to investigate the contribution of these two key matrix attributes on MCF10A migration mode phenotypes, epithelial-mesenchymal transition (EMT), and invasive potential. We developed an automated computational image analysis framework to extract migratory phenotypes from fluorescent images and determine 3D migration metrics relevant to metastatic spread. Using this analysis, we find that matrix fiber density and bulk hydrogel stiffness distinctly contribute to a variety of MCF10A migration modes including amoeboid, single mesenchymal, multicellular clusters, and collective strands. Taking advantage of the tunability of this material platform, we identify a combination of physical and soluble cues that induces distinct heterogeneous migration modes originating from the same MCF10A spheroid and use this setting to examine a functional consequence of migration mode – apoptotic resistance. We find that cells migrating as part of collective strands are more resistant to staurosporine-induced apoptosis than either disconnected multicellular clusters or individual invading cells. Improved models of the peritumoral stromal microenvironment that help elucidate relationships between matrix attributes and cell migration mode can contribute to ongoing efforts to identify efficacious cancer therapeutics that address migration plasticity-based therapy resistances.

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