2. Academic Validation
  3. Nogo-B receptor increases glycolysis and the paclitaxel resistance of estrogen receptor-positive breast cancer via the HIF-1α-dependent pathway

Nogo-B receptor increases glycolysis and the paclitaxel resistance of estrogen receptor-positive breast cancer via the HIF-1α-dependent pathway

  • Cancer Gene Ther. 2022 Oct 14. doi: 10.1038/s41417-022-00542-6.
Chang Liu 1,  Sijie Li 2,  Xiaoxiao Zhang 2,  Chunxiang Jin 3,  Baofeng Zhao 4,  Liying Li 2,  Qing Robert Miao # 5,  Ying Jin # 6,  Zhimin Fan # 7
Affiliations

Affiliations

  • 1 Department of Breast Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
  • 2 Department of Breast Surgery, The First Hospital of Jilin University, Changchun, Jilin, China.
  • 3 Institute Department of Ultrasonography, China-Japan Union Hospital of Jilin University, Changchun, China.
  • 4 CAS Key Laboratory of Separation Science for Analytical Chemistry, National Chromatographic R & A Center, Dalian Institute, Liaoning, China.
  • 5 Department of Foundations of Medicine, NYU Long Island School of Medicine, New York, NY, USA. qing.miao@nyulangone.org.
  • 6 Department of Breast Surgery, The First Hospital of Jilin University, Changchun, Jilin, China. jinying0216@jllu.edu.cn.
  • 7 Department of Breast Surgery, The First Hospital of Jilin University, Changchun, Jilin, China. fanzm@jlu.edu.cn.
  • # Contributed equally.
PMID: 36241702 DOI: 10.1038/s41417-022-00542-6
Abstract

Chemotherapy can improve the prognosis and overall survival of breast Cancer patients, but chemoresistance continues a major problem in clinical. Most breast Cancer is Estrogen Receptor (ER) positive but responds less to neoadjuvant or Adjuvant chemotherapy than ER-negative breast Cancer. The Nogo-B receptor (NgBR) increases the chemoresistance of ER-positive breast Cancer by facilitating oncogene signaling pathways. Here, we further investigated the potential role of NgBR as a novel target to overcome glycolysis-dependent paclitaxel resistance in ER-positive breast Cancer. NgBR knockdown inhibited glycolysis and promoted paclitaxel-induced Apoptosis by attenuating HIF-1α expression in ER-positive breast Cancer cells via NgBR-mediated Estrogen Receptor alpha (ERα)/hypoxia-inducible factor-1 alpha (HIF-1α) and nuclear factor-kappa B subunit (NF-κB)/HIF-1α signaling pathways. A ChIP assay further confirmed that NgBR overexpression not only facilitates ERα binding to HIF-1α and GLUT1 genes but also promotes HIF-1α binding to GLUT1, HK2, and LDHA genes, which further promotes glycolysis and induces paclitaxel resistance. In conclusion, our study suggests that NgBR expression is essential for maintaining the metabolism and paclitaxel resistance of ER-positive breast Cancer, and the NgBR can be a new therapeutic target for improving chemoresistance in ER-positive breast Cancer.

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