Inhibition of Balb/c 3T3 cell transformation by synthetic acyclic retinoid NIK-333; possible involvement of enhanced gap junctional intercellular communication

Tsujino, Takashi; Nagata, Tomoyuki; Katoh, Fumitaka; Yamasaki, Hiroshi

doi:10.1016/j.cdp.2007.06.001

Cited by 9 publications

(6 citation statements)

References 22 publications

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“…Whether NIK-333 isomerizes like ATRA to produce an isomer with properties similar to those of 9-cis-RA appears not to have been investigated. Polyprenoic acid (E5166) is cited as having RXR activity [130] and was first reported by Moriwaki, Muto, and coworkers [131]. E5166 was found to activate the CRBP-II RXRE-CAT reporter in transfected HuH-7 hepatoma cells, which constitutively express RXRα [132].…”

Section: Therapeutic Potentialmentioning

confidence: 99%

The retinoid X receptors and their ligands

Dawson

Xia

2012

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

321

325

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This chapter presents an overview of the current status of studies on the structural and molecular biology of the retinoid X receptor subtypes α, β, and γ (RXRs, NR2B1–3), their nuclear and cytoplasmic functions, post-transcriptional processing, and recently reported ligands. Points of interest are the different changes in the ligand-binding pocket induced by variously shaped agonists, the communication of the ligand–bound pocket with the coactivator binding surface and the heterodimerization interface, and recently identified ligands that are natural products, those that function as environmental toxins or drugs that had been originally designed to interact with other targets, as well as those that were deliberately designed as RXR-selective transcriptional agonists, synergists, or antagonists. Of these synthetic ligands, the general trend in design appears to be away from fully aromatic rigid structures to those containing partial elements of the flexible tetraene side chain of 9-cis-retinoic acid.

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Section: Therapeutic Potentialmentioning

confidence: 99%

The retinoid X receptors and their ligands

Dawson

Xia

2012

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

321

325

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“…16) RA has been widely used as a promoter of GJ function. 17,18) Consisting with these reports, 2-APB (2.3 µg/mL) was proved to inhibit GJ function, while RA (3 µg/mL) increased GJ function in the cells. Combination of PNS (200 µg/mL) with 2-APB does not change the function of gap junction(see Figs.…”

Section: Effects Of Pns On Gap Junction Functionmentioning

confidence: 99%

“…Treating the cells with RA, a widely used GJ promoter 17,18) for 24 h, which was verified to increase the function of Cx32/ Cx26-composing GJ (see Fig. 4), markedly reduced the cell survival only in high-density cells (Fig.…”

Section: Effects Of Gj Formation On Cytotoxicity Of Cisplatinmentioning

confidence: 99%

“…3 suggested a possible role for intercellular communication mediated by gap junctions. To test the role of GJIC in cisplatin sensitivity, experiments were performed in doxycycline-induced and doxycycline-uninduced cells, gap junction function were also manipulated by inhibition of junctional channels by 2-APB 16) and enhancement of junctional channels by RA 17,18) (Fig. 4).…”

Section: Effects Of Gj Formation On Cytotoxicity Of Cisplatinmentioning

confidence: 99%

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Panax Notoginseng Saponins Enhances the Cytotoxicity of Cisplatin <i>via</i> Increasing Gap Junction Intercellular Communication

Zhang

Yuan

et al. 2012

Biological & Pharmaceutical Bulletin

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“…Thus, the cells are released from the control regime of the tissue because GJIC impairment prevents intercellular propagation and intracellular amplification of stress stimuli. On the other hand, the dysfunction of connexins can also attenuate intercellular fluxes of harmful compounds from dysfunctional cells to their intact neighbors, leading to accumulation of toxic metabolites (such as ROS) in metabolically isolated cells (Tsujino et al, 2007;Vinken et al, 2012). Deficient/abnormal connexin expression, disturbance of connexin trafficking (Leithe, 2016), deregulated gating and selective permeability of gap junction channels may thus contribute to the accumulation of mutations in tumor cells' genome (incl.…”

Section: Connexin Deficiency and Cell Transformationmentioning

confidence: 99%

Connexin-dependent intercellular stress signaling in tissue homeostasis and tumor development

et al. 2017

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1. Connexins and gap junctions protect cells from the microenvironmental stress and are involved in propagation and intracellular processing of stress signals. 2. The quality and quantity of stress stimuli, which may lead to cell adaptation or death by apoptosis, is determined by intrinsic properties of connexins and the cell phenotype. 3. Connexin deficiency increases the resistance of tumor cells to the "outside-in" stress signaling. 4. The connexin-mediated "inside-out" stress signaling participates in tumor cell invasion during the metastatic cascade.

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Inhibition of Balb/c 3T3 cell transformation by synthetic acyclic retinoid NIK-333; possible involvement of enhanced gap junctional intercellular communication

Cited by 9 publications

References 22 publications

The retinoid X receptors and their ligands

The retinoid X receptors and their ligands

Panax Notoginseng Saponins Enhances the Cytotoxicity of Cisplatin <i>via</i> Increasing Gap Junction Intercellular Communication

Connexin-dependent intercellular stress signaling in tissue homeostasis and tumor development

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