TRPM7 regulates the migration of human nasopharyngeal carcinoma cell by mediating Ca2+ influx

Chen, Jianpeng; Luan, Yi; You, Changxuan; Chen, Xiaohua; Luo, Rong; Li, Rong

doi:10.1016/j.ceca.2010.03.003

Cited by 125 publications

(87 citation statements)

References 27 publications

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“…TRPM7 has been found to regulate cell migration and motility in diverse cell types (10,20,44,67). For example, HEK-293 cells with depleted TRPM7 migrate 56% more efficiently than the control cells in wound healing assay (66).…”

Section: Discussionmentioning

confidence: 99%

TRPM7 regulates vascular endothelial cell adhesion and tube formation

Zeng

Inoue

Sun

et al. 2015

American Journal of Physiology-Cell Physiology

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sient receptor potential melastatin 7 (TRPM7) is a nonselective cation channel with an ␣-kinase domain in its COOH terminal, known to play a role in diverse physiological and pathological processes such as Mg 2ϩ homeostasis, cell proliferation, and hypoxic neuronal injury. Increasing evidence suggests that TRPM7 contributes to the physiology/pathology of vascular systems. For example, we recently demonstrated that silencing TRPM7 promotes growth and proliferation and protects against hyperglycemia-induced injury in human umbilical vein endothelial cells (HUVECs). Here we investigated the potential effects of TRPM7 on morphology, adhesion, migration, and tube formation of vascular endothelial cells and the potential underlying mechanism. We showed that inhibition of TRPM7 function in HUVECs by silencing TRPM7 decreases the density of TRPM7-like current and cell surface area and inhibits cell adhesion to Matrigel. Silencing TRPM7 also promotes cell migration, wound healing, and tube formation. Further studies showed that the extracellular signalregulated kinase (ERK) pathway is involved in the change of cell morphology and the increase in HUVEC migration induced by TRPM7 silencing. We also demonstrated that silencing TRPM7 enhances the phosphorylation of myosin light chain (MLC) in HUVECs, which might be involved in the enhancement of cell contractility and motility. Collectively, our data suggest that the TRPM7 channel negatively regulates the function of vascular endothelial cells. Further studies on the underlying mechanism may facilitate the development of the TRPM7 channel as a target for the therapeutic intervention of vascular diseases.

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Section: Discussionmentioning

confidence: 99%

TRPM7 regulates vascular endothelial cell adhesion and tube formation

Zeng

Inoue

Sun

et al. 2015

American Journal of Physiology-Cell Physiology

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“…TRP channel-associated Ca 2+ uptake has also been shown to be stimulated by mechanical stretch of the plasma membrane associated with tension and cell shape changes occurring during migration. A specific example involves activation of TRPM7 which mediates transient and highly localized increases in intracellular [Ca 2+ ] known as Ca 2+ flickers that take place within lamellipodia in response to mechanical forces linked to contraction [11]. This initial Ca -sensitive adenylyl cyclases.…”

Section: Ion Channels and Cell Motilitymentioning

confidence: 99%

CFTR Involvement in Cell Migration and Epithelial Restitution

O’Grady¹

2017

Progress in Understanding Cystic Fibrosis

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Over the past decade, research has shown that cystic fibrosis transmembrane conductance regulator (CFTR) plays an important role in epithelial cell migration and wound healing. Experiments with airway epithelium, ovarian epithelial cells, placental epithelium and epidermal keratinocytes demonstrated that CFTR function is necessary to achieve maximum migration rates during restitution and in certain cancer cells, CFTR activity contributes to tumor cell invasion. Multiple mechanisms appear to underlie the motility-promoting actions of CFTR, and although many details remain to be established, our present understanding indicates that processes such as electrotaxis (galvanotaxis), integrin-mediated cell adhesion and lamellipodia protrusion are dependent on normal CFTR function. In this chapter, the role of CFTR in epithelial cell migration and its implications in cystic fibrosis (CF) will be reviewed with emphasis on the underlying mechanisms that may explain observations made in various epithelial tissues, particularly in airways. Ultimately, a better understanding of CFTR involvement in epithelial repair may lead to new therapeutic approaches to improve barrier function and reduce airway infection and inflammation associated with CF.

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“…Conversely, addition of a TRPM7 activator (Bradykinin) and overexpression of TRPM7 promoted the migration of 5-8F and 6-10B cells. Furthermore, the sustained Ca 2+ influx regulated by TRPM7 activated release of Ca 2+ stores via RyRs and a calcium-induced mechanism of calcium release (4).…”

Section: +mentioning

confidence: 99%