{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,9]],"date-time":"2026-03-09T08:12:00Z","timestamp":1773043920280,"version":"3.50.1"},"reference-count":36,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2020,2,12]],"date-time":"2020-02-12T00:00:00Z","timestamp":1581465600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Cellular Biochemistry"],"published-print":{"date-parts":[[2020,11]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>As an aggressive breast cancer (BCa) subtype, triple\u2010negative breast cancer (TNBC) responses poorly to chemotherapy and endocrine therapy, and usually has a worse prognosis. This is largely due to the lack of specific therapeutic targets, laying claim to an imperious demand to clarify the key signaling pathways potentiating TNBC progression. Herein, we report that expression levels of the liver\u2010specific bHLH\u2010Zip transcription factor (LISCH7), a recently identified key player in cancerous progression, preferentially enriched in TNBC in comparison with other BCa subtypes, and this upregulation was observed to be correlated to a poor survival outcome in patients with TNBC. Ablation of LISCH7 in TNBC cells impaired cell proliferation, reduced cell invasiveness, and enhanced sensitivity to the first\u2010line chemotherapeutic drug docetaxel at both in vitro and in vivo levels. Importantly, concurrent induction of <jats:italic>TGFB1<\/jats:italic>, the gene encoding transforming growth factor\u2010\u03b21 (TGF\u2010\u03b21), an essential multipluripotent regulator of TNBC, was accompanied with these alterations in cancerous properties. We further showed that LISCH7 could directly bind to the <jats:italic>TGFB1<\/jats:italic> promoter and stimulate <jats:italic>TGFB1<\/jats:italic> transcription in TNBC cells. The recruitment of LISCH7 onto the <jats:italic>TGFB1<\/jats:italic> chromatin and transactivation of <jats:italic>TGFB1<\/jats:italic> were substantially augmented by treatment with the exogenous TGF\u2010\u03b21 in a time\u2010 and dose\u2010dependent manner. Collectively, these findings suggest that LISCH7 and TGF\u2010\u03b21 form a reciprocal positive regulatory loop and cooperatively regulate cancerous progression in TNBC cells. Thus, simultaneous inhibition of both LISCH7 and TGF\u2010\u03b21 signaling may represent a more effective approach to counteract advanced TNBC.<\/jats:p>","DOI":"10.1002\/jcb.29679","type":"journal-article","created":{"date-parts":[[2020,2,12]],"date-time":"2020-02-12T12:45:48Z","timestamp":1581511548000},"page":"4642-4653","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Potentiation of cancerous progression by LISCH7 via direct stimulation of <i>TGFB1<\/i> transcription in triple\u2010negative breast cancer"],"prefix":"10.1002","volume":"121","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2445-6013","authenticated-orcid":false,"given":"Xiaojiang","family":"Tang","sequence":"first","affiliation":[{"name":"Department of Breast Surgery The First Affiliated Hospital of Xi'an Jiaotong University Xi'an 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