scholarly journals TRPV Protein Family—From Mechanosensing to Cancer Invasion

Biomolecules ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 1019
Author(s):  
Tytti Kärki ◽  
Sari Tojkander
Keyword(s):  
Cancer Progression ◽  
Intracellular Signaling ◽  
Signaling Cascades ◽  
Mechanical Stimuli ◽  
Cell Interior ◽  
Intracellular Signaling Pathways ◽  
Rapid Transmission ◽  
Critical Components ◽  
Biophysical Changes ◽  
Ca2 Channels

Biophysical cues from the cellular microenvironment are detected by mechanosensitive machineries that translate physical signals into biochemical signaling cascades. At the crossroads of extracellular space and cell interior are located several ion channel families, including TRP family proteins, that are triggered by mechanical stimuli and drive intracellular signaling pathways through spatio-temporally controlled Ca2+-influx. Mechanosensitive Ca2+-channels, therefore, act as critical components in the rapid transmission of physical signals into biologically compatible information to impact crucial processes during development, morphogenesis and regeneration. Given the mechanosensitive nature of many of the TRP family channels, they must also respond to the biophysical changes along the development of several pathophysiological conditions and have also been linked to cancer progression. In this review, we will focus on the TRPV, vanilloid family of TRP proteins, and their connection to cancer progression through their mechanosensitive nature.

scholarly journals Novel Insights into PARK7 (DJ-1), a Potential Anti-Cancer Therapeutic Target, and Implications for Cancer Progression

2020 ◽  
Vol 9 (5) ◽  
pp. 1256 ◽  
Author(s):  
Wook Jin
Keyword(s):  
Risk Factor ◽  
High Risk ◽  
Tumor Progression ◽  
Cancer Progression ◽  
Intracellular Signaling ◽  
Potential Role ◽  
Intracellular Signaling Pathways ◽  
Anti Cancer ◽  
High Risk Factor ◽  
Resistance To Chemotherapy

The expression of PARK7 is upregulated in various types of cancer, suggesting its potential role as a critical regulator of the pathogenesis of cancer and in the treatment of cancer and neurodegenerative diseases, including Parkinson’s disease, Alzheimer’s disease, and Huntington disease. PARK7 activates various intracellular signaling pathways that have been implicated in the induction of tumor progression, which subsequently enhances tumor initiation, continued proliferation, metastasis, recurrence, and resistance to chemotherapy. Additionally, secreted PARK7 has been identified as a high-risk factor for the pathogenesis and survival of various cancers. This review summarizes the current understanding of the correlation between the expression of PARK7 and tumor progression.

Caffeine stores and dopamine differentially require Ca2+ channels in goldfish somatotropes

2001 ◽  
Vol 280 (2) ◽  
pp. R494-R503 ◽  
Author(s):  
Calvin J. H. Wong ◽  
James D. Johnson ◽  
Warren K. Yunker ◽  
John P. Chang
Keyword(s):  
Intracellular Signaling ◽  
Initial Phase ◽  
Gonadotropin Releasing Hormone ◽  
Dependent Manner ◽  
Peak Response ◽  
Gh Secretion ◽  
Intracellular Signaling Pathways ◽  
Intracellular Ca ◽  
Regulation Of Growth ◽  
Ca2 Channels

The regulation of growth hormone (GH) secretion by intracellular Ca2+ stores was studied in dissociated goldfish somatotropes. We characterized a caffeine-activated intracellular store that had been shown to mediate GH release in response to gonadotropin-releasing hormone. The peak response of caffeine stimulation was reduced by ∼28% by 100 μM ryanodine in a use-dependent manner suggesting that the first 10 min of GH release is partially mediated by a caffeine-activated ryanodine receptor. The temporal sensitivities of caffeine- and dopamine-evoked GH release to blockade of Cd2+-sensitive Ca2+channels were compared. We demonstrated that the initial phase of dopamine-evoked release was dependent on Ca2+ channels, whereas the initial phase of caffeine-evoked release was sensitive only to pretreatment blockade. This would suggest that the maintenance of one class of caffeine-activated intracellular stores requires entry of Ca2+ through Cd2+-sensitive Ca2+channels. This differential temporal requirement for Ca2+channels in Ca2+ signaling may be a mechanism to segregate intracellular signaling pathways of multiple neuroendocrine regulators in the teleost pituitary.

Interrupting the FGF19-FGFR4 Axis to Therapeutically Disrupt Cancer Progression

2018 ◽  
Vol 19 (1) ◽  
pp. 17-25 ◽  
Author(s):  
Liwei Lang ◽  
Austin Y. Shull ◽  
Yong Teng
Keyword(s):  
Cancer Progression ◽  
Therapeutic Strategy ◽  
Tumor Development ◽  
Vital Role ◽  
Signaling Cascades ◽  
Cancer Cell Proliferation ◽  
Clinical Use ◽  
Fibroblast Growth ◽  
Apoptosis Resistance ◽  
Downstream Signaling

Coordination between the amplification of the fibroblast growth factor FGF19, overexpression of its corresponding receptor FGFR4, and hyperactivation of the downstream transmembrane enzyme β-klotho has been found to play pivotal roles in mediating tumor development and progression. Aberrant FGF19-FGFR4 signaling has been implicated in driving specific tumorigenic events including cancer cell proliferation, apoptosis resistance, and metastasis by activating a myriad of downstream signaling cascades. As an attractive target, several strategies implemented to disrupt the FGF19-FGFR4 axis have been developed in recent years, and FGF19-FGFR4 binding inhibitors are being intensely evaluated for their clinical use in treating FGF19-FGFR4 implicated cancers. Based on the established work, this review aims to detail how the FGF19-FGFR4 signaling pathway plays a vital role in cancer progression and why disrupting communication between FGF19 and FGFR4 serves as a promising therapeutic strategy for disrupting cancer progression.

scholarly journals Interaction of dual intracellular signaling pathways activated by the melanocortin-3 receptor.

1994 ◽  
Vol 269 (18) ◽  
pp. 13162-13166
Author(s):  
Y. Konda ◽  
I. Gantz ◽  
J. DelValle ◽  
Y. Shimoto ◽  
H. Miwa ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Intracellular Signaling ◽  
Intracellular Signaling Pathways

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

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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