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FSTL1 contribute to aggressive clinical behavior in DLBCL may by activating the DIP2A/ICAM-1-mediated adhesion

Xiping Liang1, Xiaomei Zhang1, Chaoyu Wang1

  • 1Chongqing Key Laboratory for the Mechanism and Intervention of Cancer Metastasis, Department of Hematology-Oncology, Chongqing University Cancer Hospital, Chongqing 400030, China.

Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie
|January 30, 2026
PubMed
Abstract

Insights

Elevated follistatin-like protein 1 (FSTL1) is linked to worse outcomes in diffuse large B-cell lymphoma (DLBCL). FSTL1 promotes drug resistance via a DIP2a/ICAM-1 adhesion mechanism, offering a potential therapeutic target.

Area of Science:

  • Hematology
  • Oncology
  • Molecular Biology

Background:

  • Diffuse large B-cell lymphoma (DLBCL) treatment outcomes improve with rituximab, but cell adhesion-mediated drug resistance (CAM-DR) persists.
  • The specific role of follistatin-like protein 1 (FSTL1) in CAM-DR within DLBCL remains unclear.

Purpose of the Study:

  • To investigate the association between FSTL1 expression and clinical characteristics in DLBCL patients.
  • To elucidate the underlying mechanism of FSTL1's role in DLBCL drug resistance.

Main Methods:

  • Retrospective analysis of newly diagnosed DLBCL patients treated with rituximab (2019-2024).
  • Assessment of FSTL1 expression levels and correlation with clinical features and survival outcomes.
  • In vitro experiments to evaluate FSTL1's effect on DLBCL cell behavior and drug resistance mechanisms.

Main Results:

  • FSTL1 was detected in 74.5% of DLBCL patients, with significantly elevated levels compared to controls.
  • Higher FSTL1 expression correlated with adverse clinical features (extranodal involvement, advanced stage, elevated LDH, bulky masses) and shorter overall survival (OS) and progression-free survival (PFS).
  • In vitro studies showed FSTL1 promotes DLBCL cell proliferation and vitality while decreasing antibody-dependent cellular cytotoxicity (ADCC); FSTL1 silencing reversed these effects.
  • FSTL1 was linked to CAM-DR, potentially secreted by cancer-associated fibroblasts (CAFs), interacting with DIP2A on DLBCL cells to promote ICAM-1 expression and drug resistance.

Conclusions:

  • Elevated FSTL1 levels are associated with advanced clinical characteristics and poorer outcomes in DLBCL.
  • FSTL1 contributes to DLBCL drug resistance through a DIP2a/ICAM-1-mediated adhesion mechanism.
  • FSTL1 represents a potential therapeutic target for overcoming drug resistance in DLBCL.
Keywords:
CAM-DRDLBCLFSTL1ICAM-1

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