scholarly journals Mathematical Modelling of Molecular Pathways Enabling Tumour Cell Invasion and Migration

2015 ◽  
Vol 11 (11) ◽  
pp. e1004571 ◽  
Author(s):  
David P. A. Cohen ◽  
Loredana Martignetti ◽  
Sylvie Robine ◽  
Emmanuel Barillot ◽  
Andrei Zinovyev ◽  
...  
Keyword(s):  
Mathematical Modelling ◽  
Cell Invasion ◽  
Tumour Cell ◽  
Molecular Pathways ◽  
Invasion And Migration ◽  
Tumour Cell Invasion ◽  
And Migration

scholarly journals Prediction of Mutations to Control Pathways Enabling Tumour Cell Invasion with the CoLoMoTo Interactive Notebook (Tutorial)

2018 ◽  
Author(s):  
Nicolas Levy ◽  
Aurélien Naldi ◽  
Céline Hernandez ◽  
Gautier Stoll ◽  
Denis Thieffry ◽  
...  
Keyword(s):  
Cell Invasion ◽  
Tumour Cell ◽  
Boolean Model ◽  
Software Tools ◽  
Stochastic Simulations ◽  
Invasion And Migration ◽  
Model Complex ◽  
Tumour Cell Invasion ◽  
And Migration ◽  
Model Conversion

AbstractBoolean and multi-valued logical formalisms are increasingly used to model complex cellular networks. To ease the development and analysis of logical models, a series of software tools have been proposed, often with specific assets. However, combining these tools typically implies a series of cumbersome software installation and model conversion steps. In this respect, the CoLoMoTo Interactive Notebook provides a joint distribution of several logical modelling software tools, along with an interactive web Python interface easing the chaining of complementary analyses. In this protocol, we demonstrate the assets of this approach through the analysis of a computational model of biological network. Our computational workflow combines (1) the importation of a GINsim model and its display, (2) its format conversion using the Java library BioLQM, (3) the formal prediction of mutations using the OCaml software Pint, (4) the model checking using the C++ software NuSMV, (5) quantitative stochastic simulations using the C++ software MaBoSS, and (6) the visualisation of results using the Python library matplotlib. Starting with a recent Boolean model of the signalling network controlling tumour cell invasion and migration, our model analysis culminates with the prediction of sets of mutations presumably involved in a metastatic phenotype.

scholarly journals High STRN Expression Promotes HCC Invasion and Migration but Not Cell Proliferation or Apoptosis through Facilitating Epithelial-Mesenchymal Transition

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Qian-yu Du ◽  
Jing-hao Yao ◽  
Yong-chun Zhou ◽  
Ling-jie Xu ◽  
Fu-you Zhao ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Invasion ◽  
Tumour Cell ◽  
Epithelial Mesenchymal Transition ◽  
Morphological Changes ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
Huh7 Cells ◽  
And Migration ◽  
E Cadherin

A STRN-ALK fusion protein has been recently identified as a potential therapeutic target in multiple cancers; however, the role of STRN alone in regulating the biological function of hepatocellular carcinoma (HCC) remains unclear. In this study, we firstly detected an overexpression of STRN in HCC tissues compared to that in adjacent nontumour (ANT) tissues through IHC analysis, and the expression level of this protein was positively correlated with lymph node metastasis and TNM stage. In vitro, high expression of STRN was also confirmed in different HCC cell lines, and regulation of STRN expression in Huh7 cells did not significantly affect tumour cell proliferation or apoptosis but was positively correlated with tumour cell invasion and migration capacities. Moreover, both the knockdown and overexpression of STRN in Huh7 cells can lead to cell morphological changes that are accompanied with an alteration of epithelial-mesenchymal transition (EMT) molecular markers E-cadherin and Vimentin. Finally, STRN was further proved to be negatively related to E-cadherin expression but positively related to Vimentin expression in human HCC tissue samples. Taken together, STRN is upregulated in HCC and acts as a tumour promoter regulating cell invasion and migration through facilitating the EMT process.

Methylation of ZNF331 Promotes Cell Invasion and Migration in Human Esophageal Cancer

2015 ◽  
Vol 16 (4) ◽  
pp. 322-328 ◽  
Author(s):  
Suzhen Jiang ◽  
Enqiang Linghu ◽  
Qimin Zhan ◽  
Weidong Han ◽  
Mingzhou Guo
Keyword(s):  
Esophageal Cancer ◽  
Cell Invasion ◽  
Invasion And Migration ◽  
And Migration ◽  
Human Esophageal Cancer

A Review on Phytopharmaceutical shaving Concomitant Experimental Anti-Diabetic and Anti-Cancer Effects as Potential Sources for Targeted Therapies Against Insulin Mediated Breast Cancer Cell Invasion and Migration

2020 ◽  
Vol 16 ◽  
Author(s):  
Vibhavana Singh ◽  
Rakesh Reddy ◽  
Antarip Sinha ◽  
Venkatesh Marturi ◽  
Shravani Sripathi Panditharadyula ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Medicinal Plants ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cell Invasion ◽  
Breast Tumor ◽  
Cancer Cell Invasion ◽  
Invasion And Migration ◽  
Anti Cancer ◽  
And Migration

: Diabetes and breast cancer are pathophysiologically similar and clinically established diseases that co-exist with a wider complex similar molecular signalling and having similar set of risk factors. Insulin plays a pivotal role for invasion and migration of breast cancer cells. Several ethnopharmacological evidences light the concomitant anti-diabetic and anti-cancer activity of medicinal plant and phytochemicals against breast tumor of patients with diabetes. This present article reviewed the findings on medicinal plants and phytochemicals with concomitant anti-diabetic and anti-cancer effects reported in scientific literature to facilitate the development of dual-acting therapies against diabetes and breast cancer. The schematic tabular form of published literatures on medicinal plants (63 plants belongs to 45 families) concluded the dynamics of phytochemicals against diabetes and breast tumor that could be explored further for the discovery of therapies for controlling of breast cancer cell invasion and migration in patient with diabetes.

scholarly journals Retraction Note: LncRNA miR503HG interacts with miR-31-5p through multiple ways to regulate cancer cell invasion and migration in ovarian cancer

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Ding Zhu ◽  
Xueshuang Huang ◽  
Fang Liang ◽  
Lijing Zhao
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cell ◽  
Cell Invasion ◽  
Cancer Cell Invasion ◽  
Invasion And Migration ◽  
Link Type ◽  
Retraction Notice ◽  
And Migration

This article has been retracted. Please see the Retraction Notice for more detail: 10.1186/s13048-020-00747-z

scholarly journals LncRNA MCM3AP-AS1 sponges miR-148a to enhance cell invasion and migration in small cell lung cancer

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Hua Luo ◽  
Yukun Zhang ◽  
Guangmei Qin ◽  
Bing Jiang ◽  
Lili Miao
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Cell Invasion ◽  
Small Cell ◽  
Small Cell Lung ◽  
Invasion And Migration ◽  
Protein Levels ◽  
Underlying Mechanisms ◽  
And Migration

Abstract Background MCM3AP-AS1 is a recently characterized lncRNA playing an oncogenic role in several cancers. However, its role in lung cancer remains unknown. Here, we aimed to explore the functions of MCM3AP-AS1 in small cell lung cancer (SCLC) and the possible underlying mechanisms. Methods MCM3AP-AS1 and ROCK1 levels in SCLC patients were analyzed by qPCR. RNA pull-down and luciferase assays were performed to analyze the interaction between MCM3AP-AS1 and miR-148a. ROCK1 mRNA and protein levels were detected by qPCR and Western blot, respectively. Cell invasion and migration were analyzed by Transwell assays. Results MCM3AP-AS1 was upregulated in patients with SCLC, and a high MCM3AP-AS1 level was accompanied by a low survival rate. The binding of MCM3AP-AS1 to miR-148a predicted by bioinformatics analysis was verified by RNA pull-down and luciferase assays. However, MCM3AP-AS1 and miR-148a did not affect each other’s expression. ROCK1 was upregulated in SCLC tissues and positively correlated with MCM3AP-AS1. In SCLC cells, MCM3AP-AS1 overexpression increased ROCK1 and promoted cancer cell invasion and migration, while miR-148a overexpression showed the opposite effects and attenuated the effects of MCM3AP-AS1 overexpression on ROCK1 expression and cell behaviors. Conclusions MCM3AP-AS1 sponges miR-148a, thereby increasing SCLC cell invasion and migration via upregulating ROCK1 expression.

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