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Que was selected because of its well-known anticancer effects. XBP1, on the other hand, was targeted because it has been reported to play a critical role in the progression of breast cancer and in stress-adaptive signaling. Cell viability and colony formation assays showed that Que and XBP1 silencing reduced cell growth, with the combined treatment producing a more pronounced inhibitory effect. In both cell lines, the combined treatment was associated with increased expression of apoptosis-related markers, including CASP3, CASP8 and CASP9, supporting a pro-apoptotic response. In addition, treatment-related changes were observed in EMT-associated markers, including increased CDH1 expression and decreased CDH2 expression, suggesting modulation of EMT-related molecular characteristics. Overall, these findings indicate that the combined application of XBP1 silencing and Que exerts anti-proliferative and apoptosis-associated effects on breast cancer cells and may also influence EMT-related molecular pathways. These results support the potential of combining RNAi-based approaches with plant-derived natural compounds as a therapeutic strategy for breast cancer.<\/jats:p>","DOI":"10.1007\/s13205-026-04923-8","type":"journal-article","created":{"date-parts":[[2026,6,17]],"date-time":"2026-06-17T11:15:09Z","timestamp":1781694909000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["XBP1 gene silencing augments quercetin-induced apoptosis and anti-metastatic activity in breast cancer cell lines"],"prefix":"10.1007","volume":"16","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5559-3910","authenticated-orcid":false,"given":"Sedef","family":"Ak\u00e7aalan","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3796-575X","authenticated-orcid":false,"given":"Canan","family":"Ero\u011flu G\u00fcne\u015f","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9234-1560","authenticated-orcid":false,"given":"Ercan","family":"Kurar","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,6,17]]},"reference":[{"key":"4923_CR1","doi-asserted-by":"publisher","first-page":"1773","DOI":"10.1002\/pros.20845","volume":"68","author":"R Aalinkeel","year":"2008","unstructured":"Aalinkeel R, Bindukumar B, Reynolds JL, Sykes DE, Mahajan SD, Chadha KC, Schwartz SA (2008) The dietary bioflavonoid, quercetin, selectively induces apoptosis of prostate cancer cells by down-regulating the expression of heat shock protein 90. 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