scholarly journals 911 Transient receptor potential (TRP) channels regulate cell migration of keratinocyte in vitro

2017 ◽  
Vol 137 (5) ◽  
pp. S157
Author(s):  
S. Hiroyasu ◽  
J.C.R. Jones
Keyword(s):  
Cell Migration ◽  
Transient Receptor Potential ◽  
Trp Channels ◽  
Receptor Potential ◽  
Transient Receptor

scholarly journals Transient Receptor Potential Cation Channels in Cancer Therapy

2019 ◽  
Vol 7 (12) ◽  
pp. 108 ◽  
Author(s):  
Giorgio Santoni ◽  
Federica Maggi ◽  
Maria Beatrice Morelli ◽  
Matteo Santoni ◽  
Oliviero Marinelli
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Cancer Cells ◽  
Transient Receptor Potential ◽  
Trp Channels ◽  
Receptor Potential ◽  
Chemotherapeutic Agents ◽  
Migration And Invasion ◽  
Transient Receptor

In mammals, the transient receptor potential (TRP) channels family consists of six different families, namely TRPC (canonical), TRPV (vanilloid), TRPM (melastatin), TRPML (mucolipin), TRPP (polycystin), and TRPA (ankyrin), that are strictly connected with cancer cell proliferation, differentiation, cell death, angiogenesis, migration, and invasion. Changes in TRP channels’ expression and function have been found to regulate cell proliferation and resistance or sensitivity of cancer cells to apoptotic-induced cell death, resulting in cancer-promoting effects or resistance to chemotherapy treatments. This review summarizes the data reported so far on the effect of targeting TRP channels in different types of cancer by using multiple TRP-specific agonists, antagonists alone, or in combination with classic chemotherapeutic agents, microRNA specifically targeting the TRP channels, and so forth, and the in vitro and in vivo feasibility evaluated in experimental models and in cancer patients. Considerable efforts have been made to fight cancer cells, and therapies targeting TRP channels seem to be the most promising strategy. However, more in-depth investigations are required to completely understand the role of TRP channels in cancer in order to design new, more specific, and valuable pharmacological tools.

The putative transient receptor potential channel protein encoded by the orf19.4805 gene is involved in cation sensitivity, antifungal tolerance, and filamentation in Candida albicans

2018 ◽  
Vol 64 (10) ◽  
pp. 727-731 ◽  
Author(s):  
Linghuo Jiang ◽  
Yi Yang
Keyword(s):  
Candida Albicans ◽  
Transient Receptor Potential ◽  
Trp Channels ◽  
Ion Homeostasis ◽  
Sodium Dodecyl ◽  
Receptor Potential ◽  
Antifungal Drugs ◽  
Yeast Saccharomyces Cerevisiae ◽  
Transient Receptor

Transient receptor potential (TRP) channels, an ancient family of cation channels, are highly conserved in eukaryotes and play various physiological functions, ranging from sensation of ion homeostasis to reception of pain and vision. Calcium-permeable TRP channels have been identified from the plant Arabidopsis thaliana (AtCsc1) and the budding yeast Saccharomyces cerevisiae (ScCsc1). In this study, we characterized the functions of the Csc1 homolog, orf19.4805, in Candida albicans. Orf19.4805 is a protein of 866 amino acids and 11 transmembrane domains, which shares 49% identity (69% similarity) in amino acid sequence with ScRsn1. Here, we demonstrate that deletion of the orf19.4805 gene causes C. albicans cells to be sensitive to SDS (sodium dodecyl sulfate) and antifungal drugs, and tolerance to zinc, manganese, and cadmium ions. Candida albicans cells lacking orf19.4805 show a defect in filamentation in vitro. Therefore, orf19.4805 is involved in the regulation of cation homeostasis and filamentation in C. albicans.

scholarly journals Transient Receptor Potential Channel Expression Signatures in Tumor-Derived Endothelial Cells: Functional Roles in Prostate Cancer Angiogenesis

Cancers ◽  
2019 ◽  
Vol 11 (7) ◽  
pp. 956 ◽  
Author(s):  
Michela Bernardini ◽  
Alessia Brossa ◽  
Giorgia Chinigo ◽  
Guillaume P. Grolez ◽  
Giulia Trimaglio ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Progression ◽  
Transient Receptor Potential ◽  
Trp Channels ◽  
Receptor Potential ◽  
Angiogenic Factor ◽  
Renal Tumors ◽  
Transient Receptor

Background: Transient receptor potential (TRP) channels control multiple processes involved in cancer progression by modulating cell proliferation, survival, invasion and intravasation, as well as, endothelial cell (EC) biology and tumor angiogenesis. Nonetheless, a complete TRP expression signature in tumor vessels, including in prostate cancer (PCa), is still lacking. Methods: In the present study, we profiled by qPCR the expression of all TRP channels in human prostate tumor-derived ECs (TECs) in comparison with TECs from breast and renal tumors. We further functionally characterized the role of the ‘prostate-associated’ channels in proliferation, sprout formation and elongation, directed motility guiding, as well as in vitro and in vivo morphogenesis and angiogenesis. Results: We identified three ‘prostate-associated’ genes whose expression is upregulated in prostate TECs: TRPV2 as a positive modulator of TEC proliferation, TRPC3 as an endothelial PCa cell attraction factor and TRPA1 as a critical TEC angiogenic factor in vitro and in vivo. Conclusions: We provide here the full TRP signature of PCa vascularization among which three play a profound effect on EC biology. These results contribute to explain the aggressive phenotype previously observed in PTEC and provide new putative therapeutic targets.

scholarly journals Transient Receptor Potential (TRP) Channels in Haematological Malignancies: An Update

Biomolecules ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 765
Author(s):  
Federica Maggi ◽  
Maria Beatrice Morelli ◽  
Massimo Nabissi ◽  
Oliviero Marinelli ◽  
Laura Zeppa ◽  
...  
Keyword(s):  
Transient Receptor Potential ◽  
Trp Channels ◽  
Haematological Malignancy ◽  
Receptor Potential ◽  
Progression Free Survival ◽  
Free Survival ◽  
Channel Expression ◽  
Transient Receptor

Transient receptor potential (TRP) channels are improving their importance in different cancers, becoming suitable as promising candidates for precision medicine. Their important contribution in calcium trafficking inside and outside cells is coming to light from many papers published so far. Encouraging results on the correlation between TRP and overall survival (OS) and progression-free survival (PFS) in cancer patients are available, and there are as many promising data from in vitro studies. For what concerns haematological malignancy, the role of TRPs is still not elucidated, and data regarding TRP channel expression have demonstrated great variability throughout blood cancer so far. Thus, the aim of this review is to highlight the most recent findings on TRP channels in leukaemia and lymphoma, demonstrating their important contribution in the perspective of personalised therapies.

scholarly journals The Transient Receptor Potential Vanilloid Type-2 (TRPV2) Ion Channels in Neurogenesis and Gliomagenesis: Cross-Talk between Transcription Factors and Signaling Molecules

Cancers ◽  
2019 ◽  
Vol 11 (3) ◽  
pp. 322 ◽  
Author(s):  
Giorgio Santoni ◽  
Consuelo Amantini
Keyword(s):  
Ion Channels ◽  
Neural Progenitor Cells ◽  
Transient Receptor Potential ◽  
Trp Channels ◽  
Receptor Potential ◽  
Transient Receptor Potential Vanilloid ◽  
New Therapeutic Approaches ◽  
Transient Receptor

Recently, the finding of cancer stem cells in brain tumors has increased the possibilitiesfor advancing new therapeutic approaches with the aim to overcome the limits of current availabletreatments. In addition, a role for ion channels, particularly of TRP channels, in developing neuronsas well as in brain cancer development and progression have been demonstrated. Herein, we focuson the latest advancements in understanding the role of TRPV2, a Ca2+ permeable channel belongingto the TRPV subfamily in neurogenesis and gliomagenesis. TRPV2 has been found to be expressedin both neural progenitor cells and glioblastoma stem/progenitor-like cells (GSCs). In developingneurons, post-translational modifications of TRPV2 (e.g., phosphorylation by ERK2) are required tostimulate Ca2+ signaling and nerve growth factor-mediated neurite outgrowth. TRPV2overexpression also promotes GSC differentiation and reduces gliomagenesis in vitro and in vivo.In glioblastoma, TRPV2 inhibits survival and proliferation, and induces Fas/CD95-dependentapoptosis. Furthermore, by proteomic analysis, the identification of a TRPV2 interactome-basedsignature and its relation to glioblastoma progression/recurrence, high or low overall survival anddrug resistance strongly suggest an important role of the TRPV2 channel as a potential biomarkerin glioblastoma prognosis and therapy.

scholarly journals Fine Tuning of Calcium Constitutive Entry by Optogenetically-Controlled Membrane Polarization: Impact on Cell Migration

Cells ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 1684
Author(s):  
Charles-Albert Chapotte-Baldacci ◽  
Guénaëlle Lizot ◽  
Cyrielle Jajkiewicz ◽  
Manuella Lévêque ◽  
Aubin Penna ◽  
...  
Keyword(s):  
Cell Migration ◽  
Transient Receptor Potential ◽  
Trp Channels ◽  
Receptor Potential ◽  
Calcium Entry ◽  
Fine Tuning ◽  
C2c12 Cells ◽  
Transient Receptor Potential Vanilloid ◽  
Membrane Polarization ◽  
Transient Receptor

Anomalies in constitutive calcium entry (CCE) have been commonly attributed to cell dysfunction in pathological conditions such as cancer. Calcium influxes of this type rely on channels, such as transient receptor potential (TRP) channels, to be constitutively opened and strongly depend on membrane potential and a calcium driving force. We developed an optogenetic approach based on the expression of the halorhodopsin chloride pump to study CCE in non-excitable cells. Using C2C12 cells, we found that halorhodopsin can be used to achieve a finely tuned control of membrane polarization. Escalating the membrane polarization by incremental changes in light led to a concomitant increase in CCE through transient receptor potential vanilloid 2 (TRPV2) channels. Moreover, light-induced calcium entry through TRPV2 channels promoted cell migration. Our study shows for the first time that by modulating CCE and related physiological responses, such as cell motility, halorhodopsin serves as a potentially powerful tool that could open new avenues for the study of CCE and associated cellular behaviors.

scholarly journals Linalool odor‐induced analgesia is triggered by TRPA1-independent pathway in mice

2021 ◽  
Vol 17 (1) ◽  
Author(s):  
Hideki Kashiwadani ◽  
Yurina Higa ◽  
Mitsutaka Sugimura ◽  
Tomoyuki Kuwaki
Keyword(s):  
Pain Threshold ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Analgesic Effects ◽  
Neuronal Mechanisms ◽  
Odor Exposure ◽  
Noxious Mechanical Stimulation ◽  
Transient Receptor ◽  
Deficient Mice

AbstractWe had recently reported that linalool odor exposure induced significant analgesic effects in mice and that the effects were disappeared in olfactory-deprived mice in which the olfactory epithelium was damaged, thus indicating that the effects were triggered by chemical senses evoked by linalool odor exposure. However, the peripheral neuronal mechanisms, including linalool receptors that contribute toward triggering the linalool odor-induced analgesia, still remain unexplored. In vitro studies have shown that the transient receptor potential ankyrin 1 (TRPA1) responded to linalool, thus raising the possibility that TRPA1 expressed on the trigeminal nerve terminal detects linalool odor inhaled into the nostril and triggers the analgesic effects. To address this hypothesis, we measured the behavioral pain threshold for noxious mechanical stimulation in TRPA1-deficient mice. In contrast to our expectation, we found a significant increase in the threshold after linalool odor exposure in TRPA1-deficient mice, indicating the analgesic effects of linalool odor even in TRPA1-deficient mice. Furthermore, intranasal application of TRPA1 selective antagonist did not alter the analgesic effect of linalool odor. These results showed that the linalool odor-induced analgesia was triggered by a TRPA1-independent pathway in mice.

scholarly journals RhoA enhances store-operated Ca2+ entry and intestinal epithelial restitution by interacting with TRPC1 after wounding

2015 ◽  
Vol 309 (9) ◽  
pp. G759-G767 ◽  
Author(s):  
Hee Kyoung Chung ◽  
Navneeta Rathor ◽  
Shelley R. Wang ◽  
Jian-Ying Wang ◽  
Jaladanki N. Rao
Keyword(s):  
Cell Migration ◽  
Transient Receptor Potential ◽  
Ectopic Expression ◽  
Receptor Potential ◽  
Dominant Negative ◽  
Intestinal Epithelial ◽  
Epithelial Restitution ◽  
Epithelial Cell Migration ◽  
Transient Receptor ◽  
Wounded Area

Early mucosal restitution occurs as a consequence of epithelial cell migration to resealing of superficial wounds after injury. Our previous studies show that canonical transient receptor potential-1 (TRPC1) functions as a store-operated Ca2+ channel (SOC) in intestinal epithelial cells (IECs) and plays an important role in early epithelial restitution by increasing Ca2+ influx. Here we further reported that RhoA, a small GTP-binding protein, interacts with and regulates TRPC1, thus enhancing SOC-mediated Ca2+ entry (SOCE) and epithelial restitution after wounding. RhoA physically associated with TRPC1 and formed the RhoA/TRPC1 complexes, and this interaction increased in stable TRPC1-transfected IEC-6 cells (IEC-TRPC1). Inactivation of RhoA by treating IEC-TRPC1 cells with exoenzyme C3 transferase (C3) or ectopic expression of dominant negative RhoA (DNMRhoA) reduced RhoA/TRPC1 complexes and inhibited Ca2+ influx after store depletion, which was paralleled by an inhibition of cell migration over the wounded area. In contrast, ectopic expression of wild-type (WT)-RhoA increased the levels of RhoA/TRPC1 complexes, induced Ca2+ influx through activation of SOCE, and promoted cell migration after wounding. TRPC1 silencing by transfecting stable WT RhoA-transfected cells with siRNA targeting TRPC1 (siTRPC1) reduced SOCE and repressed epithelial restitution. Moreover, ectopic overexpression of WT-RhoA in polyamine-deficient cells rescued the inhibition of Ca2+ influx and cell migration induced by polyamine depletion. These findings indicate that RhoA interacts with and activates TRPC1 and thus stimulates rapid epithelial restitution after injury by inducing Ca2+ signaling.

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