{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,12]],"date-time":"2026-10-12T13:40:36Z","timestamp":1791812436343,"version":"4.3.4"},"reference-count":59,"publisher":"National Academy of Sciences","issue":"39","license":[{"start":{"date-parts":[[2022,9,20]],"date-time":"2022-09-20T00:00:00Z","timestamp":1663632000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2022,9,27]]},"abstract":"<jats:p>\n                    Triple-negative breast cancer (TNBC) is the most challenging breast cancer subtype for its high rates of relapse, great metastatic potential, and short overall survival. How cancer cells acquire metastatic potency through the conversion of noncancer stem-like cells into cancer cells with stem-cell properties is poorly understood. Here, we identified the long noncoding RNA (lncRNA) TGFB2-AS1 as an important regulator of the reversibility and plasticity of noncancer stem cell populations in TNBC. We revealed that TGFB2-AS1 impairs the breast cancer stem-like cell (BCSC) traits of TNBC cells in\u00a0vitro and dramatically decreases tumorigenic frequency and lung metastasis in\u00a0vivo. Mechanistically, TGFB2-AS1 interacts with SMARCA4, a core subunit of the SWI\/SNF chromatin remodeling complex, and results in transcriptional repression of its target genes including\n                    <jats:italic>TGFB2<\/jats:italic>\n                    and\n                    <jats:italic>SOX2<\/jats:italic>\n                    in an\n                    <jats:italic>in cis<\/jats:italic>\n                    or\n                    <jats:italic>in trans<\/jats:italic>\n                    way, leading to inhibition of transforming growth factor \u03b2 (TGF\u03b2) signaling and BCSC characteristics. In line with this, TGFB2-AS1 overexpression in an orthotopic TNBC mouse model remarkably abrogates the enhancement of tumor growth and lung metastasis endowed by TGF\u03b22. Furthermore, combined prognosis analysis of TGFB2-AS1 and TGF\u03b22 in TNBC patients shows that high TGFB2-AS1 and low TGF\u03b22 levels are correlated with better outcome. These findings demonstrate a key role of TGFB2-AS1 in inhibiting disease progression of TNBC based on switching the cancer cell fate of TNBC and also shed light on the treatment of TNBC patients.\n                  <\/jats:p>","DOI":"10.1073\/pnas.2117988119","type":"journal-article","created":{"date-parts":[[2022,9,20]],"date-time":"2022-09-20T13:50:47Z","timestamp":1663681847000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":52,"title":["TGFB2-AS1 inhibits triple-negative breast cancer progression via interaction with SMARCA4 and regulating its targets\n                    <i>TGFB2<\/i>\n                    and\n                    <i>SOX2<\/i>"],"prefix":"10.1073","volume":"119","author":[{"given":"Cixiang","family":"Zhou","sequence":"first","affiliation":[{"name":"State Key Lab of Oncogene and Related Genes, Renji Hospital, Shanghai Institute of Cancer, Key Lab of Cell Differentiation and Apoptosis of Ministry of Education, 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