Carbon monoxide: A new player in the redox regulation of connexin hemichannels

Retamal, Mauricio A.; León-Paravic, Carmen G.; Ezquer, Marcelo; Ezquer, Fernando; Rio, Rodrigo Del; Pupo, Amaury; Martı́nez, Agustı́n D.; González, Carlos

doi:10.1002/iub.1388

Cited by 15 publications

(8 citation statements)

References 160 publications

(190 reference statements)

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“…Carbon monoxide is emerging as a promising molecule to treat several diseases including cancer. It can directly or indirectly inhibit the function of connexin hemichannels [ 117 , 118 ] although the role of hemichannels in cancer cells is yet to be uncovered. Ganoderma lucidum , an herbal mushroom increases Cx43 expression and inhibits growth of human ovarian cancer cells, and this growth inhibition was abrogated by knocking down Cx43 gene [ 119 ].…”

Section: Connexin Channels In Clinical Studies and Potential Cancer Tmentioning

confidence: 99%

Connexin and pannexin channels in cancer

Jiang

Peñuela

2016

BMC Cell Biol

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Communication among cells via direct cell-cell contact by connexin gap junctions, or between cell and extracellular environment via pannexin channels or connexin hemichannels, is a key factor in cell function and tissue homeostasis. Upon malignant transformation in different cancer types, the dysregulation of these connexin and pannexin channels and their effect in cellular communication, can either enhance or suppress tumorigenesis and metastasis. In this review, we will highlight the latest reports on the role of the well characterized connexin family and its ability to form gap junctions and hemichannels in cancer. We will also introduce the more recently discovered family of pannexin channels and our current knowledge about their involvement in cancer progression.

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Section: Connexin Channels In Clinical Studies and Potential Cancer Tmentioning

confidence: 99%

Connexin and pannexin channels in cancer

Jiang

Peñuela

2016

BMC Cell Biol

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“…CO is well known as a toxic molecule, because CO binds with high affinity to hemoglobin, resulting in hypoxia [52]. It has been well established that CO-induced hypoxia is a potentially a major mechanism of COP-induced neuronal damage in the acute phase [52,53]. The pathomechanism of COP-induced delayed neuropsychiatric sequelae is probably more complex than that of CO-induced hypoxia, since the former presents as recurrent severe neuropsychiatric symptoms that recur after an interval of apparent normality following the apparent resolution of acute symptoms [54].…”

Section: Discussionmentioning

confidence: 99%

Amantadine Combines Astroglial System Xc− Activation with Glutamate/NMDA Receptor Inhibition

et al. 2019

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A glutamate/NMDA receptor (NMDA-R) antagonist, amantadine (AMA) exhibits a broad spectrum of clinically important properties, including antiviral, antiparkinsonian, neuroprotective, neuro-reparative and cognitive-enhancing effects. However, both clinical and pre-clinical studies have demonstrated that noncompetitive NMDA-R antagonists induce severe schizophrenia-like cognitive deficits. Therefore, this study aims to clarify the clinical discrepancy between AMA and noncompetitive NMDA-R antagonists by comparing the effects of AMA with those of a noncompetitive NMDA-R antagonist, MK801, on rat tripartite glutamatergic synaptic transmission using microdialysis and primary cultured astrocytes. Microdialysis study demonstrated that the stimulatory effects of AMA on L-glutamate release differed from those of MK801 in the globus pallidus, entorhinal cortex and entopeduncular nucleus. The stimulatory effect of AMA on L-glutamate release was modulated by activation of cystine/glutamate antiporter (Sxc). Primary cultured astrocytes study demonstrated that AMA also enhanced glutathione synthesis via Sxc activation. Furthermore, carbon-monoxide induced damage of the astroglial glutathione synthesis system was repaired by AMA but not MK801. Additionally, glutamate/AMPA receptor (AMPA-R) antagonist, perampanel enhanced the protective effects of AMA. The findings of microdialysis and cultured astrocyte studies suggest that a combination of Sxc activation with inhibitions of ionotropic glutamate receptors contributes to neuroprotective, neuro-reparative and cognitive-enhancing activities that can mitigate several neuropsychiatric disorders.

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“…For Cx43 Hcs in cancer development, carbon monoxide (CO), a promising molecule to treat several diseases including cancer has been shown to inhibit their function [ 155 ]. CO donors inhibit Hc uptake in tumour cell lines (MCF-7 and HeLa cells) expressing exogenous Cx43 or Cx46 [ 156 ].…”

Section: Connexin and Pannexin Channels In Potential Cancer Therapmentioning

confidence: 99%

Connexins and Pannexins: Important Players in Tumorigenesis, Metastasis and Potential Therapeutics

Graham

Jiang

Mesnil

2018

IJMS

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Since their characterization more than five decades ago, gap junctions and their structural proteins—the connexins—have been associated with cancer cell growth. During that period, the accumulation of data and molecular knowledge about this association revealed an apparent contradictory relationship between them and cancer. It appeared that if gap junctions or connexins can down regulate cancer cell growth they can be also implied in the migration, invasion and metastatic dissemination of cancer cells. Interestingly, in all these situations, connexins seem to be involved through various mechanisms in which they can act either as gap-junctional intercellular communication mediators, modulators of signalling pathways through their interactome, or as hemichannels, which mediate autocrine/paracrine communication. This complex involvement of connexins in cancer progression is even more complicated by the fact that their hemichannel function may overlap with other gap junction-related proteins, the pannexins. Despite this complexity, the possible involvements of connexins and pannexins in cancer progression and the elucidation of the mechanisms they control may lead to use them as new targets to control cancer progression. In this review, the involvements of connexins and pannexins in these different topics (cancer cell growth, invasion/metastasis process, possible cancer therapeutic targets) are discussed.

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Carbon monoxide: A new player in the redox regulation of connexin hemichannels

Cited by 15 publications

References 160 publications

Connexin and pannexin channels in cancer

Connexin and pannexin channels in cancer

Amantadine Combines Astroglial System Xc− Activation with Glutamate/NMDA Receptor Inhibition

Connexins and Pannexins: Important Players in Tumorigenesis, Metastasis and Potential Therapeutics

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