ArticleMolecular oncology2022
Growth arrest-specific protein 2 (GAS2) interacts with CXCR4 to promote T-cell leukemogenesis partially via c-MYC.
Article in Molecular oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- GAS2 Co-Expression Networks in Breast Cancer: Identification of Potential Biomarkers and Therapeutic Targets.Advanced pharmaceutical bulletin · 2026Article
- A novel regulatory circuit of ATG4B and SESN3 promotes T cell leukemogenesis.Journal of experimental & clinical cancer research : CR · 2025Article
- Review
- Insights into Structure and Function of Growth Arrest Specific 2 (GAS2).Journal of Cancer · 2025Review
- CXCR4 regulates macrophage M1 polarization by altering glycolysis to promote prostate fibrosis.Cell communication and signaling : CCS · 2024Article
Corrections and comments
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although growth arrest-specific protein 2 (GAS2) promotes the growth of T-cell acute lymphoblastic leukemia (T-ALL) cells in culture, the effect of GAS2 on T-cell leukemogenesis has not been studied, and the mechanism remains unclear. In the present study, xenograft studies showed that GAS2 silencing impaired T-cell leukemogenesis and decreased leukemic cell infiltration. Mechanistically, GAS2 regulated the protein expression of C-X-C chemokine receptor type 4 (CXCR4) rather than its transcript expression. Immunoprecipitation revealed that GAS2 interacted with CXCR4, and confocal analysis showed that GAS2 was partially co-expressed with CXCR4, which provided a strong molecular basis for GAS2 to regulate CXCR4 expression. Importantly, CXCR4 overexpression alleviated the inhibitory effect of GAS2 silencing on the growth and migration of T-ALL cells. Moreover, GAS2 or CXCR4 silencing inhibited the expression of NOTCH1 and c-MYC. Forced expression of c-MYC rescued the growth suppression induced by GAS2 or CXCR4 silencing. Meanwhile, GAS2 deficiency, specifically in blood cells, had a mild effect on normal hematopoiesis, including T-cell development, and GAS2 silencing did not affect the growth of normal human CD3
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