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Voltage-gated Sodium Channel SCN5A Promotes Tumor Progression and Enhances Chemosensitivity to 5-Fluorouracil in Colorectal Cancer

ABSTRACT: Voltage-gated Sodium Channel SCN5A Promotes Tumor Progression and Enhances Chemosensitivity to 5-Fluorouracil in Colorectal Cancer

PROVIDER: PRJNA631241 | ENA |

REPOSITORIES: ENA

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Voltage-gated Sodium Channel SCN5A Promotes Tumor Progression and Enhances Chemosensitivity to 5-Fluorouracil in Colorectal Cancer

Project description:SCN5A was reported to promote proliferation and invasiveness potential in colorectal cancer, yet the mechanism was not clarified, and little was known about its association with chemosensitivity to 5-fluorouracil. In the current study, elevated SCN5A expression were associated with poor prognosis and metastasis in colorectal cancers, whereas stage II-III patients with up-regulated SCN5A expression were more likely to benefit from 5-fluorouracil-based adjuvant chemotherapy. SCN5A could promote proliferation and invasiveness potential through regulating cell cycle and epithelial-mesenchymal transition in colorectal cancer cells. Furthermore, SCN5A regulated Ras signaling by stabilizing KRas-calmodulin complex through Ca2+ influx. Apart from that, under 5-fluorouracil treatment, SCN5A promoted calmodulin-dependent apoptosis in colorectal cancers.

2020-05-09 | GSE150134 | GEO

Regulation of fin regeneration by a voltage-gated sodium channel

Project description:Regulation of fin regeneration by a voltage-gated sodium channel

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Impact of the Voltage-Gated Calcium Channel Antagonist Nimodipinedipine on the Development of Oligodendrocyte Precursor Cells

Project description:We investigated the effects of nimodipine, a L-type voltage-gated calcium channel antagonist, on the expression profile of myelin genes in the oligodendrocyte precursor cell (OPC) line Oli-Neu. We performed gene expression profiling analysis using data obtained from RNA-seq of four biological replicates for treatment and four replicates for control condition.

2023-03-30 | GSE221939 | GEO

Roles of voltage-gated potassium channels in the maintenance of pancreatic cancer stem cells

Project description:The targeting of membrane proteins that are activated in cancer stem cells (CSCs) represents one of the key strategies in novel cancer therapy. The present study investigated ion channel expression profiles and functions in pancreatic CSCs (PCSCs). Cells strongly expressing aldehyde dehydrogenase 1 family member A1 (ALDH1A1) were separated from PK59 cells, a human pancreatic cancer cell line, using fluorescence-activated cell sorting (FACS), and PCSCs were identified based on tumorsphere formation. A microarray analysis was performed to investigate gene expression profiles in PCSCs. ALDH1A1 messenger RNA levels were higher in PCSCs. PCSCs were resistant to 5-fluorouracil (5-FU) and capable of re-differentiation. The microarray analysis revealed that gene expression related to ion channels, including voltage-gated potassium channels (Kv), was up-regulated. 4-Aminopyridine (4-AP), a potent Kv inhibitor, exhibited greater cytotoxicity in PCSCs. In a xenograft model in nude mice, tumor volumes were significantly smaller in mice injected with PK59 cells treated with 4-AP than in those injected with non-treated cells. The present results implicate Kv in the persistence of PCSCs, and the Kv inhibitor, 4-AP, has potential as a therapeutic agent for pancreatic carcinoma.

2021-04-16 | GSE172185 | GEO

Severe deficiency of voltage-gated sodium channel NaV1.2 elevates neuronal excitability in adult mice

Project description:Scn2a encodes voltage-gated sodium channel NaV1.2, a main mediator of neuronal action potential firing. The current paradigm suggests that NaV1.2 gain-of-function variants enhance neuronal excitability resulting in epilepsy, whereas NaV1.2 deficiency impairs excitability contributing to autism. This paradigm, however, does not explain why 20~30% of patients with NaV1.2 deficiency still develop seizures. Here we report a counterintuitive finding that severe NaV1.2 deficiency results in increased neuronal excitability. Using a unique NaV1.2-deficient mouse model, we found enhanced intrinsic excitabilities of principal neurons in the prefrontal cortex and striatum, brain regions known to be involved in Scn2a-related seizures. This increased excitability is autonomous, and is reversible by the genetic restoration of Scn2a expression in adult mice. RNA-sequencing revealed that the downregulation of multiple potassium channels including KV1.1, and KV channel openers alleviated hyperexcitability of NaV1.2-deficient neurons. This unexpected neuronal hyperexcitability may serve as a cellular basis underlying NaV1.2 deficiency-related seizures.

2021-07-13 | GSE179818 | GEO

Severe deficiency of voltage-gated sodium channel NaV1.2 elevates neuronal excitability in adult mice

Project description:Severe deficiency of voltage-gated sodium channel NaV1.2 elevates neuronal excitability in adult mice

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Roles of voltage-gated potassium channels in the maintenance of pancreatic cancer stem cells

Project description:Roles of voltage-gated potassium channels in the maintenance of pancreatic cancer stem cells

| PRJNA722320 | ENA

Kv7.2 LC-MSMS - Updating in vivo and in vitro phosphorylation and methylation sites of voltage-gated Kv7

Project description:Voltage-gated Kv7.2 potassium channels regulate neuronal excitability. The gating of Kv7 channels is regulated by various mediators and neurotransmitters acting via G protein-coupled receptors; the underlying signalling cascades involve phosphatidylinositol-4,5-bisphosphate (PIP2), Ca2+/Calmodulin and phosphorylation. Recent studies have reported that PIP2 sensitivity of Kv7.2 channels is affected by two PTMs, phosphorylation and methylation, harboured in the PIP2 binding domains. Here this project aimed to update phosphorylation and methylation sites on Kv7.2 from heterologous cells, the rat brain and GST-fusion Kv7.2 N- and C-terminal ends proteins.

2017-08-25 | PXD005567 | Pride

MicroRNA-96 is required to prevent allodynia by repressing voltage-gated sodium channels in spinal cord

Project description:Voltage-gated sodium channels (Navs) 1.7, 1.8, and 1.9 are predominately expressed in peripheral sensory neurons and are critical for action potential propagation in nociceptors. Unexpectedly, we found that expression of SCN9A, SCN10A, SCN11A, and SCN2A, the alpha subunit of Nav1.7, Nav1.8, Nav1.9 and Nav1.2, respectively, are up-regulated in spinal dorsal horn (SDH) neurons of miR-96 knockout mice. These mice also have de-repression of CACNA2d1/2 in DRG and display heat and mechanical allodynia that could be attenuated by intrathecal or intraperitoneal injection of Nav1.7 or Nav1.8 inhibitors or Gabapentin. Moreover, Gad2::CreERT2 conditional miR-96 knockout mice phenocopied global knockout mice, implicating inhibitory neurons; nerve injury induced significant loss of miR-96 in SDH GABAergic and Glutamatergic neurons in mice which negative correlated to up-regulation of Nav1.7, Nav1.8, Nav1.9 and Scn2a, this dis-regulation of miR-96 and Navs in SDH neurons contributed to neuropathic pain which can be alleviated by intrathecal injection of Nav1.7 or Nav1.8 blockers. In conclusion, miR-96 is required to avoid allodynia through limiting the expression of VGCCs and Navs in DRG and Navs in SDH in naïve and nerve injury induced neuropathic pain mice. Our findings suggest that central nervous system penetrating Nav1.7 and Nav1.8 inhibitors may be efficacious for pain relief.

2021-07-06 | GSE144832 | GEO

MicroRNA-96 is required to prevent allodynia by repressing voltage-gated sodium channels in spinal cord

Project description:MicroRNA-96 is required to prevent allodynia by repressing voltage-gated sodium channels in spinal cord

| PRJNA605099 | ENA