Related Experiment Video
Updated: Jun 4, 2026
A Three-dimensional Model of Spheroids to Study Colon Cancer Stem Cells
Published on: January 22, 2021
Colon Adenocarcinoma Cell-Derived Galectins-1,3 Modulate Differentiation of CD4+ T Lymphocytes In Vitro
V S Poletika1, G V Reingardt2, A V Kurnosenko3,2
1Siberian State Medical University, Ministry of Health of the Russian Federation, Tomsk, Russia. vpoletika@yandex.ru.
Abstract:
We investigated how selective inhibition of galectin-1 and galectin-3 expressed by COLO 201 colorectal adenocarcinoma cells modulates CD4+ T lymphocyte differentiation in vitro. The mRNA expression levels of the transcription factors T-bet (TBX21), RORC2, and Foxp3 were analyzed in peripheral blood mononuclear cells (PBMCs) from colorectal cancer patients and healthy donors following co-culture with COLO 201 cells in the presence of galectin-1 inhibitor OTX 008, galectin-3 inhibitor GB1107, or both. Inhibition of galectin-1 in co-cultures increased TBX21 and RORC2 mRNA expression while suppressing FOXP3 in PBMCs from both groups. In patient-derived PBMCs, galectin-3 inhibition produced a similar effect. Conversely, in healthy donor cells, galectin-3 blockade suppressed RORC2 and induced FOXP3 expression. Notably, the most pronounced downregulation of FOXP3 was achieved by simultaneously inhibiting both galectins.
Insights
Selective inhibition of galectin-1 and galectin-3 in colorectal cancer cells impacts CD4+ T lymphocyte differentiation. Blocking both galectins significantly reduced FOXP3 expression in T cells.
Area of Science:
- Immunology
- Cancer Biology
- Molecular Biology
Background:
- Galectins, particularly galectin-1 and galectin-3, are implicated in cancer progression and immune modulation.
- Colorectal adenocarcinoma cells express galectins that can influence the tumor microenvironment.
- CD4+ T lymphocyte differentiation is crucial for adaptive immunity and is often dysregulated in cancer.
Purpose of the Study:
- To investigate the effect of selective galectin-1 and galectin-3 inhibition on CD4+ T lymphocyte differentiation.
- To analyze the impact of these inhibitors on key transcription factors (T-bet, RORC2, Foxp3) in T cells from colorectal cancer patients and healthy donors.
Main Methods:
- Co-culture of COLO 201 colorectal adenocarcinoma cells with peripheral blood mononuclear cells (PBMCs) from colorectal cancer patients and healthy donors.
- Treatment with galectin-1 inhibitor (OTX 008), galectin-3 inhibitor (GB1107), or both inhibitors.
- Analysis of mRNA expression levels of T-bet (TBX21), RORC2, and Foxp3 transcription factors in PBMCs using quantitative PCR.
Main Results:
- Inhibition of galectin-1 increased TBX21 and RORC2 mRNA expression while decreasing FOXP3 mRNA expression in PBMCs from both patient and healthy donor groups.
- Galectin-3 inhibition in patient-derived PBMCs showed similar effects to galectin-1 inhibition.
- In healthy donor PBMCs, galectin-3 blockade suppressed RORC2 and induced FOXP3 expression.
- Simultaneous inhibition of both galectin-1 and galectin-3 resulted in the most significant downregulation of FOXP3 expression.
Conclusions:
- Selective inhibition of galectin-1 and galectin-3 differentially modulates CD4+ T lymphocyte differentiation.
- The combined inhibition of galectin-1 and galectin-3 holds potential for reprogramming T cell responses in the context of colorectal cancer.
- Targeting galectins may offer a therapeutic strategy to influence the immune microenvironment in colorectal adenocarcinoma.
