2. Academic Validation
  3. Cell adhesion molecule CD44v10 promotes stem-like properties in triple-negative breast cancer cells via glucose transporter GLUT1-mediated glycolysis

Cell adhesion molecule CD44v10 promotes stem-like properties in triple-negative breast cancer cells via glucose transporter GLUT1-mediated glycolysis

  • J Biol Chem. 2022 Oct 12;102588. doi: 10.1016/j.jbc.2022.102588.
Qian Guo 1,  Yaqi Qiu 1,  Yiwen Liu 2,  Yiqing He 2,  Guoliang Zhang 2,  Yan Du 2,  Cuixia Yang 1,  Feng Gao 3
Affiliations

Affiliations

  • 1 Department of Molecular Biology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, 600 Yishan Road, Shanghai 200233, China; Department of Clinical Laboratory, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, 600 Yishan Road, Shanghai 200233, China.
  • 2 Department of Molecular Biology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, 600 Yishan Road, Shanghai 200233, China.
  • 3 Department of Molecular Biology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, 600 Yishan Road, Shanghai 200233, China; Department of Clinical Laboratory, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, 600 Yishan Road, Shanghai 200233, China. Electronic address: [email protected].
PMID: 36243113 DOI: 10.1016/j.jbc.2022.102588
Abstract

Cell adhesion molecule CD44v8-10 is associated with tumor stemness and malignancy, however, whether CD44v10 alone confers these properties is unknown. Here, we demonstrated that CD44v10 promotes stemness and chemoresistance of triple-negative breast cancers (TNBCs) individually. Next, we identified that genes differentially expressed in response to ectopic expression of CD44v10 are mostly related to glycolysis. Further, we showed that CD44v10 upregulates glucose transporter 1 (GLUT1) to facilitate glycolysis by activating the MAPK/ERK and PI3K/Akt signaling pathways. This glycolytic reprogramming induced by CD44v10 contributes to the stem-like properties of TNBC cells and confers resistance to paclitaxel (PTX) treatment. Notably, we determined that the knockdown of GLUT1 could attenuate the enhanced effects of CD44v10 on glycolysis, stemness, and PTX resistance. Collectively, our findings provide novel insights into the function of CD44v10 in TNBCs and suggest that targeting CD44v10 may contribute to future clinical therapy.

Keywords

CD44v10; GLUT1; Glycolysis; Stem cell-like property; Triple-negative breast cancer.

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