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Disco-interacting protein 2 homolog A (EC (DIP2 homolog A) [C21orf106] [DIP2] [KIAA0184]


Blocking the FSTL1-DIP2A Axis Improves Anti-tumor Immunity.

Immune dysfunction is a strong factor in the resistance of cancer to treatment. Blocking immune checkpoint pathways is a promising approach to improve anti-tumor immunity, but the clinical efficacies are still limited. We previously identified follistatin-like 1 (FSTL1) as a determinant of immune dysfunction mediated by mesenchymal stromal/stem cells (MSCs) and immunoregulatory cells. Here, we demonstrate that blocking FSTL1 but not immune checkpoint pathways significantly suppresses cancer progression and metastasis in several mouse tumor models with increased MSCs. Expression of DIP2A (the receptor of FSTL1) in tumor cells is critical for FSTL1-induced immunoresistance. FSTL1/DIP2A co-positivity in tumor tissues correlates with poor prognosis in NSCLC patients. Thus, breaking the FSTL1-DIP2A axis may be a useful strategy for successfully inducing anti-tumor immunity.

MeSH Terms

  • Animals
  • Carcinoma, Non-Small-Cell Lung
  • Carrier Proteins
  • Case-Control Studies
  • Cell Line, Tumor
  • Cell Movement
  • Cell Proliferation
  • Disease Progression
  • Female
  • Follistatin-Related Proteins
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Immunity, Innate
  • Lung Neoplasms
  • Male
  • Mesenchymal Stem Cells
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Nuclear Proteins
  • Prognosis
  • RNA, Small Interfering
  • Signal Transduction
  • Survival Analysis
  • Tumor Burden
  • Xenograft Model Antitumor Assays


  • FSTL1
  • aging
  • antibody
  • cancer metastasis
  • immune checkpoint
  • immune exhaustion
  • immunosuppression
  • lung cancer
  • mesenchymal stromal/stem cells