SMARCA4/2 loss inhibits chemotherapy-induced apoptosis by restricting IP3R3-mediated Ca2+ flux to mitochondria View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2021-09-13

AUTHORS

Yibo Xue, Jordan L. Morris, Kangning Yang, Zheng Fu, Xianbing Zhu, Fraser Johnson, Brian Meehan, Leora Witkowski, Amber Yasmeen, Tunde Golenar, Mackenzie Coatham, Geneviève Morin, Anie Monast, Virginie Pilon, Pierre Olivier Fiset, Sungmi Jung, Anne V. Gonzalez, Sophie Camilleri-Broet, Lili Fu, Lynne-Marie Postovit, Jonathan Spicer, Walter H. Gotlieb, Marie-Christine Guiot, Janusz Rak, Morag Park, William Lockwood, William D. Foulkes, Julien Prudent, Sidong Huang

ABSTRACT

Inactivating mutations in SMARCA4 and concurrent epigenetic silencing of SMARCA2 characterize subsets of ovarian and lung cancers. Concomitant loss of these key subunits of SWI/SNF chromatin remodeling complexes in both cancers is associated with chemotherapy resistance and poor prognosis. Here, we discover that SMARCA4/2 loss inhibits chemotherapy-induced apoptosis through disrupting intracellular organelle calcium ion (Ca2+) release in these cancers. By restricting chromatin accessibility to ITPR3, encoding Ca2+ channel IP3R3, SMARCA4/2 deficiency causes reduced IP3R3 expression leading to impaired Ca2+ transfer from the endoplasmic reticulum to mitochondria required for apoptosis induction. Reactivation of SMARCA2 by a histone deacetylase inhibitor rescues IP3R3 expression and enhances cisplatin response in SMARCA4/2-deficient cancer cells both in vitro and in vivo. Our findings elucidate the contribution of SMARCA4/2 to Ca2+-dependent apoptosis induction, which may be exploited to enhance chemotherapy response in SMARCA4/2-deficient cancers. More... »

PAGES

5404

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  • Journal

    TITLE

    Nature Communications

    ISSUE

    1

    VOLUME

    12

    Author Affiliations

    Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s41467-021-25260-9

    DOI

    http://dx.doi.org/10.1038/s41467-021-25260-9

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1141074059

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/34518526


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    71 schema:description Inactivating mutations in SMARCA4 and concurrent epigenetic silencing of SMARCA2 characterize subsets of ovarian and lung cancers. Concomitant loss of these key subunits of SWI/SNF chromatin remodeling complexes in both cancers is associated with chemotherapy resistance and poor prognosis. Here, we discover that SMARCA4/2 loss inhibits chemotherapy-induced apoptosis through disrupting intracellular organelle calcium ion (Ca<sup>2+</sup>) release in these cancers. By restricting chromatin accessibility to ITPR3, encoding Ca<sup>2+</sup> channel IP3R3, SMARCA4/2 deficiency causes reduced IP3R3 expression leading to impaired Ca<sup>2+</sup> transfer from the endoplasmic reticulum to mitochondria required for apoptosis induction. Reactivation of SMARCA2 by a histone deacetylase inhibitor rescues IP3R3 expression and enhances cisplatin response in SMARCA4/2-deficient cancer cells both in vitro and in vivo. Our findings elucidate the contribution of SMARCA4/2 to Ca<sup>2+</sup>-dependent apoptosis induction, which may be exploited to enhance chemotherapy response in SMARCA4/2-deficient cancers.
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