IL-1 Induces p62/SQSTM1 and Autophagy in ERα⁺/PR⁺ BCa Cell Lines Concomitant with ERα and PR Repression, Conferring an ERα⁻/PR⁻ BCa-Like Phenotype

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dc.contributor.authorNawas, Afshan Fathima
dc.contributor.authorMistry, Ragini
dc.contributor.authorNarayanan, Shrinath
dc.contributor.authorThomas-Jardin, Shayna Elizabeth
dc.contributor.authorRamachandran, Janani
dc.contributor.authorRavichandran, Jananisree
dc.contributor.authorNeduvelil, Ebin
dc.contributor.authorLuangpanh, Krisha
dc.contributor.authorDelk, Nikki A.
dc.contributor.utdAuthorNawas, Afshan Fathima
dc.contributor.utdAuthorMistry, Ragini
dc.contributor.utdAuthorNarayanan, Shrinath
dc.contributor.utdAuthorThomas-Jardin, Shayna Elizabeth
dc.contributor.utdAuthorRamachandran, Janani
dc.contributor.utdAuthorRavichandran, Jananisree
dc.contributor.utdAuthorNeduvelil, Ebin
dc.contributor.utdAuthorLuangpanh, Krisha
dc.contributor.utdAuthorDelk, Nikki A.
dc.date.accessioned2020-10-19T21:44:09Z
dc.date.available2020-10-19T21:44:09Z
dc.date.issued2019-02
dc.descriptionDue to copyright restrictions and/or publisher's policy full text access from Treasures at UT Dallas is limited to current UTD affiliates (use the provided Link to Article).
dc.description.abstractEstrogen receptor α (ERα)ˡᵒʷ/⁻ tumors are associated with breast cancer (BCa) endocrine resistance, where ERα low tumors show a poor prognosis and a molecular profile similar to triple negative BCa tumors. Interleukin-1 (IL-1) downregulates ERα accumulation in BCa cell lines, yet the cells can remain viable. In kind, IL-1 and ERα show inverse accumulation in BCa patient tumors and IL-1 is implicated in BCa progression. IL-1 represses the androgen receptor hormone receptor in prostate cancer cells concomitant with the upregulation of the prosurvival, autophagy-related protein, Sequestome-1 (p62/SQSTM1; hereinafter, p62); and given their similar etiology, we hypothesized that IL-1 also upregulates p62 in BCa cells concomitant with hormone receptor repression. To test our hypothesis, BCa cell lines were exposed to conditioned medium from IL-1-secreting bone marrow stromal cells (BMSCs), IL-1, or IL-1 receptor antagonist. Cells were analyzed for the accumulation of ERα, progesterone receptor (PR), p62, or the autophagosome membrane protein, microtubule-associated protein 1 light chain 3 (LC3), and for p62-LC3 interaction. We found that IL-1 is sufficient to mediate BMSC-induced ERα and PR repression, p62 and autophagy upregulation, and p62-LC3 interaction in ERα⁺/PR⁺ BCa cell lines. However, IL-1 does not significantly elevate the high basal p62 accumulation or high basal autophagy in the ERα⁻/PR⁻ BCa cell lines. Thus, our observations imply that IL-1 confers a prosurvival ERα⁻/PR⁻ molecular phenotype in ERα⁺/PR⁺ BCa cells that may be dependent on p62 function and autophagy and may underlie endocrine resistance.
dc.description.departmentSchool of Natural Sciences and Mathematics
dc.description.sponsorshipNational Institutes of Health, National Cancer Institute, Grant/Award Numbers:K01CA160602, R21CA17579
dc.identifier.bibliographicCitationNawas, Afshan Fathima, Ragini Mistry, Shrinath Narayanan, Shayna Elizabeth Thomas-Jardin, et al. 2019. "IIL-1 Induces p62/SQSTM1 and Autophagy in ERα⁺/PR⁺ BCa Cell Lines Concomitant with ERα and PR Repression, Conferring an ERα⁻/PR⁻ BCa-Like Phenotype." Journal of Cellular Biochemistry 120(2): 1477-1491, doi: 10.1002/jcb.27340
dc.identifier.issn0730-2312
dc.identifier.issue2
dc.identifier.urihttps://dx.doi.org/10.1002/jcb.27340
dc.identifier.urihttps://hdl.handle.net/10735.1/9037
dc.identifier.volume120
dc.language.isoen
dc.publisherWiley
dc.rights©2018 Wiley Periodicals, Inc.
dc.source.journalJournal of Cellular Biochemistry
dc.subjectInterleukin-1
dc.subjectSQSTM1 protein, human
dc.subjectProstate—Cancer
dc.subjectBreast—Cancer
dc.subjectEstrogen—Receptors
dc.subject.meshAutophagy
dc.subject.meshReceptors, Estrogen
dc.subject.meshP62 protein, human
dc.subject.meshHydroxychloroquine
dc.subject.meshTemozolomide
dc.titleIL-1 Induces p62/SQSTM1 and Autophagy in ERα⁺/PR⁺ BCa Cell Lines Concomitant with ERα and PR Repression, Conferring an ERα⁻/PR⁻ BCa-Like Phenotype
dc.type.genrearticle

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