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While many studies have investigated molecular dysregulation by hotspot mutations at Y537 and D538, which exhibit an estrogen-independent constitutively active phenotype, the functional abnormalities of other mutations remain obscure. The K303R mutation in primary invasive BC has been implicated with endocrine resistance, tumor size, and lymph node positivity. However, the impact of the K303R mutation on the cell epigenome is yet unknown.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Methods and results<\/jats:title>\n                <jats:p>We introduced the K303R ER\u03b1 mutant in ER\u03b1-negative MDA-MB-453 cells to monitor ER\u03b1-dependent transactivation and to perform epigenomic analyses. ATAC-seq and ChIP-Seq analyses indicated that both wild-type (WT) and the K303R mutant associated with Forkhead box (Fox) protein family motif regions at similar rates, even without an ER\u03b1-binding sequence, but only the K303R mutant induced chromatin opening at those regions. Biochemical analyses demonstrated that the WT and the K303R mutant can be tethered on DNA by FoxA1 indirectly, but only the K303R\/FoxA1\/DNA complex can induce associations with the nuclear receptor cofactor 2 (NCOA2).<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Conclusions<\/jats:title>\n                <jats:p>These findings suggest that the K303R mutant induces chromatin opening at the Fox binding region through the FoxA1-dependent associations of the K303R mutant to NCOA2 and then probably disrupts the regulation of Fox-target genes, resulting in K303R-related BC events.<\/jats:p>\n              <\/jats:sec>","DOI":"10.1007\/s11033-022-08089-3","type":"journal-article","created":{"date-parts":[[2022,11,27]],"date-time":"2022-11-27T20:59:20Z","timestamp":1669582760000},"page":"1209-1220","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Estrogen receptor \u03b1 K303R mutation reorganizes its binding to forkhead box protein A1 regions and induces chromatin opening"],"prefix":"10.1007","volume":"50","author":[{"given":"Tomoyoshi","family":"Nakadai","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Liying","family":"Yang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kohei","family":"Kumegawa","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Reo","family":"Maruyama","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2022,11,27]]},"reference":[{"issue":"688\u201394","key":"8089_CR1","first-page":"696","volume":"26","author":"E Lim","year":"2012","unstructured":"Lim E, Metzger-Filho O, Winer EP (2012) The natural history of hormone receptor-positive breast cancer. 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