Site specific hypermethylation of CpGs in Connexin genes30,26and43in different grades of glioma and attenuated levels of their mRNAs

Jothi, Jayalakshmi; Vanisree, Arambakkam Janardhanam; Ravisankar, Shantha; Rama, Kumara

doi:10.1080/00207454.2018.1526802

Cited by 6 publications

(2 citation statements)

References 36 publications

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“…transcription factors (including AP2) are likely to have a role in regulating the expression of Gjb2 and Gjb6 (Common et al, 2005;Jayalakshmi et al, 2019). Furthermore, Gjb2 is upregulated by AP2 in normal tissue (Tu et al, 2001;Adam and Cyr, 2016).…”

Section: Discussionmentioning

confidence: 99%

Activin/Nodal/TGF-β Pathway Inhibitor Accelerates BMP4-Induced Cochlear Gap Junction Formation During in vitro Differentiation of Embryonic Stem Cells

Fukunaga

Cheng

et al. 2021

Front. Cell Dev. Biol.

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Mutations in gap junction beta-2 (GJB2), the gene that encodes connexin 26 (CX26), are the most frequent cause of hereditary deafness worldwide. We recently developed an in vitro model of GJB2-related deafness (induced CX26 gap junction-forming cells; iCX26GJCs) from mouse induced pluripotent stem cells (iPSCs) by using Bone morphogenetic protein 4 (BMP4) signaling-based floating cultures (serum-free culture of embryoid body-like aggregates with quick aggregation cultures; hereafter, SFEBq cultures) and adherent cultures. However, to use these cells as a disease model platform for high-throughput drug screening or regenerative therapy, cell yields must be substantially increased. In addition to BMP4, other factors may also induce CX26 gap junction formation. In the SFEBq cultures, the combination of BMP4 and the Activin/Nodal/TGF-β pathway inhibitor SB431542 (SB) resulted in greater production of isolatable CX26-expressing cell mass (CX26+ vesicles) and higher Gjb2 mRNA levels than BMP4 treatment alone, suggesting that SB may promote BMP4-mediated production of CX26+ vesicles in a dose-dependent manner, thereby increasing the yield of highly purified iCX26GJCs. This is the first study to demonstrate that SB accelerates BMP4-induced iCX26GJC differentiation during stem cell floating culture. By controlling the concentration of SB supplementation in combination with CX26+ vesicle purification, large-scale production of highly purified iCX26GJCs suitable for high-throughput drug screening or regenerative therapy for GJB2-related deafness may be possible.

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Section: Discussionmentioning

confidence: 99%

Activin/Nodal/TGF-β Pathway Inhibitor Accelerates BMP4-Induced Cochlear Gap Junction Formation During in vitro Differentiation of Embryonic Stem Cells

Fukunaga

Cheng

et al. 2021

Front. Cell Dev. Biol.

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“…Cnxs were reported to be epigenetically regulated by hypermethylation of the promoter or acetylation/deacetilation of histones. For example, the extent and site specificity of Cnx 26 and 30 methylation were found to correspond with the grade of glioma [28] and Cnx 45 methylation was indicated in colorectal cancer [29].…”

Section: Connexin Synthesismentioning

confidence: 99%

The Multifaceted Role of Connexins in Tumor Microenvironment Initiation and Maintaining

Kutova¹,

Pospelov²,

Balalaeva³

2021

Preprint

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The modern paradigm of studying the processes of carcinogenesis and vital activity of tumor tissues implies increased attention to constituents of tumor microenvironment (TME) and their interactions. These interactions between the cells in TME can be mediated via protein junctions of different types. Connexins (Cnxs) are one of the major contributors to intercellular communication. They form gap junctions responsible for the transfer of ions, metabolites, peptides, miRNA, etc. between neighboring tumor cells as well as between tumor and stromal cells. Cnx hemichannels mediate purinergic signaling and bidirectional molecular transport with the extracellular environment. Additionally, Cnxs were reported to localize in tumor-derived exosomes and facilitate the release of their cargo. A large body of evidence implies that the role of connexins in cancer is multifaceted. Pro- or anti-tumorigenic properties of connexins are determined by their abundance, localization and functionality as well as channel assembly and non-channel functions. In this review we have summarized the data on the Cnxs contribution in TME and to the cancer initiation and progression.

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Cellular and Molecular Mechanisms of Tumor Promotion

Bode,

Zhang

2024

Reference Module in Biomedical Sciences

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Site specific hypermethylation of CpGs in Connexin genes30,26and43in different grades of glioma and attenuated levels of their mRNAs

Cited by 6 publications

References 36 publications

Activin/Nodal/TGF-β Pathway Inhibitor Accelerates BMP4-Induced Cochlear Gap Junction Formation During in vitro Differentiation of Embryonic Stem Cells

Activin/Nodal/TGF-β Pathway Inhibitor Accelerates BMP4-Induced Cochlear Gap Junction Formation During in vitro Differentiation of Embryonic Stem Cells

The Multifaceted Role of Connexins in Tumor Microenvironment Initiation and Maintaining

Cellular and Molecular Mechanisms of Tumor Promotion

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