ArticleHaematologica2010
Thalidomide decreases gelatinase production by malignant B lymphoid cell lines through disruption of multiple integrin-mediated signaling pathways.
Article in Haematologica, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Involvement of interferon γ-producing mast cells in immune responses against melanocytes in vitiligo requires Mas-related G protein-coupled receptor X2 activation.Chinese medical journal · 2025Article
- Adhesion molecules in multiple myeloma oncogenesis and targeted therapy.International journal of hematologic oncology · 2022Review
- Repurposing of thalidomide and its derivatives for the treatment of SARS-coV-2 infections: Hints on molecular action.British journal of clinical pharmacology · 2021Article
- Molecular Targets in Hepatocarcinogenesis and Implications for Therapy.Journal of clinical medicine · 2018Review
- Thalidomide promotes transplanted cell engraftment in the rat liver by modulating inflammation and endothelial integrity.Journal of hepatology · 2016Article
- Thyroid hormone regulates adhesion, migration and matrix metalloproteinase 9 activity via αvβ3 integrin in myeloma cells.Oncotarget · 2014Article
- Mechanism of immunomodulatory drugs' action in the treatment of multiple myeloma.Acta biochimica et biophysica Sinica · 2014Review
- The rise, fall and subsequent triumph of thalidomide: lessons learned in drug development.Therapeutic advances in hematology · 2011Article
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThalidomide and its analogs are effective agents in the treatment of multiple myeloma. Since gelatinases (matrix metalloproteinases-2 and -9) play a crucial role in tumor progression, we explored the effect of thalidomide on gelatinase production by malignant B lymphoid cell lines. DESIGN AND
methodsWe investigated the effect of therapeutic doses of thalidomide on integrin-mediated production of gelatinases by malignant B lymphoid cell lines by gelatin zymography, western-blot, reverse transcriptase polymerase chain reaction and invasive capacity through Matrigel-coated Boyden chambers. We also explored the effect of thalidomide on the activation status of the main signaling pathways involved in this process.
resultsThalidomide strongly inhibited gelatinase production by B-cell lines and primary myeloma cells in response to fibronectin, the most efficient gelatinase inducer identified in lymphoid cells. Thalidomide disrupted integrin-mediated signaling pathways involved in gelatinase induction and release, such as Src and MAP-kinase ERK activation, resulting in decreased cell motility and invasiveness. Unexpectedly, treatment with thalidomide elicited an increase in fibronectin-induced Akt phosphorylation through phosphoinositide 3-kinase-independent pathways since thalidomide decreased fibronectin-induced phosphoinositide 3-kinase phosphorylation and reversed the inhibition of Akt phosphorylation achieved by the phosphoinositide 3-kinase inhibitors wortmannin and LY294002.
conclusionsDisruption of integrin-mediated signaling may be an important mechanism through which thalidomide and its analogs impair tumor cell interactions with the microenvironment. The unexpected effects of thalidomide on Akt activation indicate the need for further studies to elucidate whether the interference with Akt downstream effects would synergize with the anti-tumor activity of thalidomide.
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