2. Academic Validation
  3. HMGN5 escorts oncogenic STAT3 signaling by regulating the chromatin landscape in breast cancer tumorigenesis

HMGN5 escorts oncogenic STAT3 signaling by regulating the chromatin landscape in breast cancer tumorigenesis

  • Mol Cancer Res. 2022 Sep 6;MCR-22-0241. doi: 10.1158/1541-7786.MCR-22-0241.
Jiahui Mou 1,  Meijun Huang 2,  Feifei Wang 3,  Xiaoding Xu 3,  Hanqi Xie 4,  Henglei Lu 1,  Mingyang Li 2,  Yu Li 1,  Weiwen Kong 1,  Jing Chen 1,  Ying Xiao 5,  Yiding Chen 6,  Chaochen Wang 7,  Jin Ren 1
Affiliations

Affiliations

  • 1 Shanghai Institute of Materia Medica, China.
  • 2 Zhejiang University School of Medicine, China.
  • 3 Nanjing University of Chinese Medicine, China.
  • 4 Zhejiang University School of Medicine, Haining, China.
  • 5 Sir Run Run Shaw Hospital, China.
  • 6 The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
  • 7 Second Affiliated Hospital of Zhejiang University, Hangzhou, Zhejiang, China.
PMID: 36066963 DOI: 10.1158/1541-7786.MCR-22-0241
Abstract

Cancer progression is highly dependent on the ability of Cancer cell tumor formation, in which epigenetic modulation plays an essential role. However, the epigenetic factors promoting breast tumor formation are less known. Screened from 3D-sphere tumor formation model, HMGN5 which regulates chromatin structures became the candidate therapeutic target in breast Cancer, though its role is obscure. HMGN5 is highly expressed in 3D-spheres of breast Cancer cells and clinical tumors, also an unfavorable prognostic marker in patients. Furthermore, HMGN5 controls tumor formation and metastasis of breast Cancer cells in vitro and in vivo. Mechanistically, HMGN5 is governed by active STAT3 transcriptionally and further escorts STAT3 to shape the oncogenic chromatin landscape and transcriptional program. More importantly, interference of HMGN5 by nanoparticle-packaged siRNA effectively inhibits tumor growth in breast Cancer cell-derived xenograft mice model. Implications: Our findings reveal a novel feed-forward circuit between HMGN5 and STAT3 in promoting breast Cancer tumorigenesis and suggest HMGN5 as a novel epigenetic therapeutic target in STAT3-hyperactive breast Cancer.

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