{"entity": "publication", "iuid": "a445fcf02c4c4b7ba85491f3e393a206", "timestamp": "2026-10-11T13:53:33.211Z", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/a445fcf02c4c4b7ba85491f3e393a206.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/a445fcf02c4c4b7ba85491f3e393a206"}}, "title": "Estrogen Receptor Beta Influences the Inflammatory p65 Cistrome in Colon Cancer Cells.", "authors": [{"family": "Indukuri", "given": "Rajitha", "initials": "R"}, {"family": "Hases", "given": "Linnea", "initials": "L"}, {"family": "Archer", "given": "Amena", "initials": "A"}, {"family": "Williams", "given": "Cecilia", "initials": "C"}], "type": "journal article", "published": "2021-03-30", "journal": {"title": "Front Endocrinol (Lausanne)", "issn": "1664-2392", "volume": "12", "pages": "650625", "issn-l": "1664-2392"}, "abstract": "Inflammation is a primary component of both initiation and promotion of colorectal cancer (CRC). Cytokines secreted by macrophages, including tumor necrosis factor alpha (TNF\u03b1), activates the pro-survival transcription factor complex NF\u03baB. The precise mechanism of NF\u03baB in CRC is not well studied, but we recently reported the genome-wide transcriptional impact of TNF\u03b1 in two CRC cell lines. Further, estrogen signaling influences inflammation in a complex manner and suppresses CRC development. CRC protective effects of estrogen have been shown to be mediated by estrogen receptor beta (ER\u03b2, ESR2), which also impacts inflammatory signaling of the colon. However, whether ER\u03b2 impacts the chromatin interaction (cistrome) of the main NF\u03baB subunit p65 (RELA) is not known. We used p65 chromatin immunoprecipitation followed by sequencing (ChIP-Seq) in two different CRC cell lines, HT29 and SW480, with and without expression of ER\u03b2. We here present the p65 colon cistrome of these two CRC cell lines. We identify that RELA and AP1 motifs are predominant in both cell lines, and additionally describe both common and cell line-specific p65 binding sites and correlate these to transcriptional changes related to inflammation, migration, apoptosis and circadian rhythm. Further, we determine that ER\u03b2 opposes a major fraction of p65 chromatin binding in HT29 cells, but enhances p65 binding in SW480 cells, thereby impacting the p65 cistrome differently in the two cell lines. However, the biological functions of the regulated genes appear to have similar roles in both cell lines. To our knowledge, this is the first time the p65 CRC cistrome is compared between different cell lines and the first time an influence by ER\u03b2 on the p65 cistrome is investigated. Our work provides a mechanistic foundation for a better understanding of how estrogen influences inflammatory signaling through NF\u03baB in CRC cells.", "doi": "10.3389/fendo.2021.650625", "pmid": "33859619", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC8042384"}], "notes": [], "created": "2026-09-23T12:53:51.176Z", "modified": "2026-09-23T12:53:51.201Z"}