Integrin expression and glycosylation patterns regulate cell-matrix adhesion and alter with breast cancer progression

Singh, Chandrajeet; Shyanti, Ritis K.; Singh, Virendra; Kale, R.K.; Mishra, Jai P.N.; Singh, Rana P.

doi:10.1016/j.bbrc.2018.03.169

Cited by 47 publications

(31 citation statements)

References 25 publications

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“…The glycosylation is a key modification observed in different types of cancers, including breast, ovarian, and prostate cancers [ 48 ]. Glycosylation facilitates the cell adhesion, proliferation, and metastasis of breast cancer [ 49 ]. Six glycosylated genes—FUT1, FUCA1, POFUT1, MAN1A1, RPN1 and DPM1—are reported to be associated with the prognosis of breast cancer [ 50 ].…”

Section: Greb1 Structure and Functionmentioning

confidence: 99%

Role for Growth Regulation by Estrogen in Breast Cancer 1 (GREB1) in Hormone-Dependent Cancers

Cheng

Michalski

Kommagani

2018

IJMS

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Sex hormones play important roles in the onset and progression of several cancers, such as breast, ovarian, and prostate cancer. Although drugs targeting sex hormone function are useful in treating cancer, tumors often develop resistance. Thus, we need to define the downstream effectors of sex hormones in order to develop new treatment strategies for these cancers. Recent studies unearthed one potential mediator of steroid hormone action in tumors: growth regulation by estrogen in breast cancer 1 (GREB1). GREB1 is an early estrogen-responsive gene, and its expression is correlated with estrogen levels in breast cancer patients. Additionally, GREB1 responds to androgen in prostate cancer cells, and can stimulate the proliferation of breast, ovarian, and prostate cancer cells. Recent studies have shown that GREB1 also responds to progesterone in human endometrial cells, suggesting that GREB1 is a pan steroid-responsive gene. This mini-review examines evidence that GREB1 participates in several hormone-dependent cancers and could be targeted to treat these cancers.

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Section: Greb1 Structure and Functionmentioning

confidence: 99%

Role for Growth Regulation by Estrogen in Breast Cancer 1 (GREB1) in Hormone-Dependent Cancers

Cheng

Michalski

Kommagani

2018

IJMS

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“…Tumor metastasis is one of the major problems in cancer therapy and urgently requires more effective control [ 14 ]. Among metastasis-associated genes, integrins mediate cell-cell as well as tumor cell-extracellular matrix crosstalk by exchanging signals across cellular membranes of cancer cells [ 15 ]. Integrins are heterodimers consisting of 8β and 18α subunits.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-183-5p Inhibits Aggressiveness of Cervical Cancer Cells by Targeting Integrin Subunit Beta 1 (ITGB1)

Zhang

Liu

et al. 2018

Med Sci Monit

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BackgroundAccumulating studies demonstrate that microRNAs play crucial roles in multiple processes of cancer progression. Lower levels of miR-183 have ben observed in diverse types of tumors but the mechanism and precise function of miR-183-5p in cervical cancer have largely not been investigated.Material/MethodsThe level of miR-183-5p in different cervical cancer cell lines and clinical tissues was detected qRT-PCR assays. Transwell and wound-healing migration assays were conducted to assess the functional roles of miR-183-5p in over-expressing cervical cancer cells in vitro. Rescue assays were carried out to confirm the contribution of integrin subunit Beta 1 (ITGB1) to the aggressiveness of cancer cells regulated by miR-183-5p.ResultsmiR-183-5p was reduced in clinical tissues of cervical cancer and cell lines when compared to the normal subjects and normal cervical epithelial cell line, respectively. In addition, over-expression of miR-183-5p markedly inhibited migration and invasion in cervical cancer cells, and increased aggressiveness was observed in miR-183-5p inhibitor transfected cells. Furthermore, the luciferase reporter assays revealed that ITGB1 was the gene directly regulated by miR-183-5p. Notably, a negative association between the ITGB1 and miR-183-5p was found, and the gene expressions of ITGB1 was mediated by miR-183-5p in cervical cancer cells.ConclusionsmiR-183-5p serves as a latent anti-oncogene by targeting the metastasis-promoter gene, ITGB1.

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“…Fig 7 shows how this analysis can be used to determine the best strategies of altering matrix properties to change the cell migration behavior. A similar analysis can be performed on an n-parameter space including cellular and matrix mechanical properties, providing insight into how these properties should be managed in vivo using existing methods to remodel or disrupt the ECM structure[ 46 – 49 ] or modify cellular polarization [ 24 ], integrin expression [ 46 , 50 ], or pseudopod protrusion frequency [ 51 ]. This versatility, incorporation of many possible cell-matrix interaction parameters, and the ability to rapidly simulate long-term cell migration for a large number of cells are the key strengths of the proposed algorithm and the described simulation platform.…”

Section: Discussionmentioning

confidence: 99%

A stochastic algorithm for accurately predicting path persistence of cells migrating in 3D matrix environments

Yeoman

Katira

2018

PLoS ONE

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Cell mobility plays a critical role in immune response, wound healing, and the rate of cancer metastasis and tumor progression. Mobility within a three-dimensional (3D) matrix environment can be characterized by the average velocity of cell migration and the persistence length of the path it follows. Computational models that aim to predict cell migration within such 3D environments need to be able predict both of these properties as a function of the various cellular and extra-cellular factors that influence the migration process. A large number of models have been developed to predict the velocity of cell migration driven by cellular protrusions in 3D environments. However, prediction of the persistence of a cell’s path is a more tedious matter, as it requires simulating cells for a long time while they migrate through the model extra-cellular matrix (ECM). This can be a computationally expensive process, and only recently have there been attempts to quantify cell persistence as a function of key cellular or matrix properties. Here, we propose a new stochastic algorithm that can simulate and analyze 3D cell migration occurring over days with a computation time of minutes, opening new possibilities of testing and predicting long-term cell migration behavior as a function of a large variety of cell and matrix properties. In this model, the matrix elements are generated as needed and stochastically based on the biophysical and biochemical properties of the ECM the cell migrates through. This approach significantly reduces the computational resources required to track and calculate cell matrix interactions. Using this algorithm, we predict the effect of various cellular and matrix properties such as cell polarity, cell mechanoactivity, matrix fiber density, matrix stiffness, fiber alignment, and fiber binding site density on path persistence of cellular migration and the mean squared displacement of cells over long periods of time.

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Integrin expression and glycosylation patterns regulate cell-matrix adhesion and alter with breast cancer progression

Cited by 47 publications

References 25 publications

Role for Growth Regulation by Estrogen in Breast Cancer 1 (GREB1) in Hormone-Dependent Cancers

Role for Growth Regulation by Estrogen in Breast Cancer 1 (GREB1) in Hormone-Dependent Cancers

MicroRNA-183-5p Inhibits Aggressiveness of Cervical Cancer Cells by Targeting Integrin Subunit Beta 1 (ITGB1)

A stochastic algorithm for accurately predicting path persistence of cells migrating in 3D matrix environments

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