Novel Therapeutic Approaches of Ion Channels and Transporters in Cancer

Ramírez, Ana; García-Quiroz, Janice; Aguilar-Eslava, Luis; Sánchez-Pérez, Yesennia; Camacho, Javier

doi:10.1007/112_2020_28

Cited by 10 publications

(11 citation statements)

References 394 publications

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“…Recent studies have described that altered expression or activity of ion transporters play an important role in the development or progression of different types of cancer [ 22 , 23 , 24 , 25 , 26 ]. For this reason, many ion transporters emerged as potential targets for cancer therapy [ 27 , 28 ]. Our study demonstrates, for the first time, that smoking affects cell proliferation in BE in which the ubiquitously expressed transmembrane transporter, NHE-1, plays a central role.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of NHE-1 Increases Smoke-Induced Proliferative Activity of Barrett’s Esophageal Cell Line

Becskeházi

Korsós

Gál

et al. 2021

IJMS

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Several clinical studies indicate that smoking predisposes its consumers to esophageal inflammatory and malignant diseases, but the cellular mechanism is not clear. Ion transporters protect esophageal epithelial cells by maintaining intracellular pH at normal levels. In this study, we hypothesized that smoking affects the function of ion transporters, thus playing a role in the development of smoking-induced esophageal diseases. Esophageal cell lines were treated with cigarettesmoke extract (CSE), and the viability and proliferation of the cells, as well as the activity, mRNA and protein expression of the Na+/H+ exchanger-1 (NHE-1), were studied. NHE-1 expression was also investigated in human samples. For chronic treatment, guinea pigs were exposed to tobacco smoke, and NHE-1 activity was measured. Silencing of NHE-1 was performed by using specific siRNA. CSE treatment increased the activity and protein expression of NHE-1 in the metaplastic cells and decreased the rate of proliferation in a NHE-1-dependent manner. In contrast, CSE increased the proliferation of dysplastic cells independently of NHE-1. In the normal cells, the expression and activity of NHE-1 decreased due to in vitro and in vivo smoke exposure. Smoking enhances the function of NHE-1 in Barrett’s esophagus, and this is presumably a compensatory mechanism against this toxic agent.

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Section: Discussionmentioning

confidence: 99%

Inhibition of NHE-1 Increases Smoke-Induced Proliferative Activity of Barrett’s Esophageal Cell Line

Becskeházi

Korsós

Gál

et al. 2021

IJMS

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“…Accordingly, the use of antihistamines has shown promising effects to fight this pathology, as in the case of astemizole, a non-sedating second-generation antihistamine, commonly prescribed for the treatment of allergies. This drug has been repurposed as an antineoplastic agent, since in addition to H1-histamine receptors blockade, it targets several other molecules involved in cancer development, such as P-glycoprotein and the voltage-gated potassium channels EAG1 and human EAG related genes (HERG) [ 212 ]. Regarding BC, astemizole has shown to exert antiproliferative effects against both hormone-dependent and non-hormone-dependent BC cell lines, as well as in primary cell cultures derived from breast tumors [ 21 , 83 ].…”

Section: Calcitriol In Combination With Histamine Inhibitors In Bcmentioning

confidence: 99%

Combinations of Calcitriol with Anticancer Treatments for Breast Cancer: An Update

Segovia-Mendoza

García-Quiroz

Díaz

et al. 2021

IJMS

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Preclinical, clinical, and epidemiological studies indicate that vitamin D3 (VD) deficiency is a risk factor for the development of breast cancer. Underlying mechanisms include the ability of calcitriol to induce cell differentiation, inhibit oncogenes expression, and modify different signaling pathways involved in the control of cell proliferation. In addition, calcitriol combined with different kinds of antineoplastic drugs has been demonstrated to enhance their beneficial effects in an additive or synergistic fashion. However, a recognized adjuvant regimen based on calcitriol for treating patients with breast cancer has not yet been fully established. Accordingly, in the present work, we review and discuss the preclinical and clinical studies about the combination of calcitriol with different oncological drugs, aiming to emphasize its main therapeutic benefits and opportunities for the treatment of this pathology.

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“…KCNJ/Kir is a subset of K + channels, comprising seven subfamilies in four functional groups: classical KCNJ/Kir channels, G protein-gated KCNJ/Kir channels, KCNJ/KATP (referred to as ATP-sensitive potassium channels) [ 11 ], and KCNJ/K + -transport channels. All these channels require phosphatidylinositol(4,5)-bisphosphate (PtdIns [ 4 , 5 ]P 2 ) for the activation and transportation of K + in cells. KCNJ/Kir channels are widely distributed in the heart, brain, ventricular structures, and pancreas, located in cellular membrane net systems, and they stabilize resting membrane potential.…”

Section: Types Of Ion Channelsmentioning

confidence: 99%

“…This process is called store-operated calcium entry (SOCE) [ 19 ]. In contrast, ITPR is an ER Ca 2+ channel activated by inositol-(1,4,5)-trisphosphate (Ins [ 1 , 4 , 5 ]P 3 ), leading to the release of Ca 2+ from the ER into the cytoplasm and mitochondria via the ER-mitochondria contact site. SOCE is typically activated by the engagement of G protein-coupled receptors or a tyrosine kinase cascade to activate PLC (phospholipase C) to cleave PtdIns(4,5)P 2 and produce Ins(1,4,5)P 3 /InsP3.…”

Section: Types Of Ion Channelsmentioning

confidence: 99%

“…This dynamic modulation is mediated by several types of transport proteins, especially ion channels or transporters, which broadly distribute in impermeable cellular membranes, including those of the mitochondria, the endoplasmic reticulum (ER), Golgi apparatus (GA), endosomes, and lysosomes. Ion channels and transporters allow the ions (e.g., calcium [Ca 2+ ], potassium [K + ], sodium [Na + ], and chloride [Cl − ]) to influx and efflux across lipid membrane barriers [ 4 ]. Ion channels are integral pore-forming membrane proteins, which enable passive transport of ions through the membrane to reduce their electrochemical gradient [ 5 ].…”

Section: Introductionmentioning

confidence: 99%

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Ion Channels and Transporters in Autophagy

et al. 2021

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Ion exchange between intracellular and extracellular spaces is the basic mechanism for controlling cell metabolism and signal transduction. This process is mediated by ion channels and transporters on the plasma membrane, or intracellular membranes that surround various organelles, in response to environmental stimuli. Macroautophagy (hereafter referred to as autophagy) is one of the lysosomal-dependent degradation pathways that maintains homeostasis through the degradation and recycling of cellular components (e.g., dysfunctional proteins and damaged organelles). Although autophagy-related (ATG) proteins play a central role in regulating the formation of autophagy-related member structures (e.g., phagophores, autophagosomes, and autolysosomes), the autophagic process also involves changes in expression and function of ion channels and transporters. Here we discuss current knowledge of the mechanisms that regulate autophagy in mammalian cells, with special attention to the ion channels and transporters. We also highlight prospects for the development of drugs targeting ion channels and transporters in autophagy.

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Novel Therapeutic Approaches of Ion Channels and Transporters in Cancer

Cited by 10 publications

References 394 publications

Inhibition of NHE-1 Increases Smoke-Induced Proliferative Activity of Barrett’s Esophageal Cell Line

Inhibition of NHE-1 Increases Smoke-Induced Proliferative Activity of Barrett’s Esophageal Cell Line

Combinations of Calcitriol with Anticancer Treatments for Breast Cancer: An Update

Ion Channels and Transporters in Autophagy

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