ArticleMolecular oncology2020
The brain acid-soluble protein 1 (BASP1) interferes with the oncogenic capacity of MYC and its binding to calmodulin.
Article in Molecular oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 28 citations in OpenAlex.
- Reactivation of the silencedProceedings of the National Academy of Sciences of the United States of America · 2026Article
- From inflammation to remodelling: A novel BASP1Journal of advanced research · 2025Article
- Article
- Increased Sirtuin 6 Activity in Tumor Cells Can Prompt CD4-Positive T-Cell Differentiation Into Regulatory T Cells and Impede Immune Surveillance in the Microenvironment.World journal of oncology · 2025Article
- Advances in RNA Labeling with Trifluoromethyl Groups.Chemistry (Weinheim an der Bergstrasse, Germany) · 2023Article
- BASP1 expression is associated with poor prognosis and is correlated with immune infiltration in gastric cancer.FEBS open bio · 2023Article
- Article
- BASP1 promotes high glucose-induced endothelial apoptosis in diabetes via activation of EGFR signaling.Journal of diabetes investigation · 2023Article
- Strategies to target the cancer driver MYC in tumor cells.Frontiers in oncology · 2023Review
- BASP1 is a prognostic biomarker associated with immunotherapeutic response in head and neck squamous cell carcinoma.Frontiers in oncology · 2023Article
- Garlic exosome-like nanoparticles reverse high-fat diet induced obesity via the gut/brain axis.Theranostics · 2022Article
- Cholesterol is required for transcriptional repression by BASP1.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- The Diarylheptanoid Curcumin Induces MYC Inhibition and Cross-Links This Oncoprotein to the Coactivator TRRAP.Frontiers in oncology · 2021Article
- MYC Analysis in Cancer and Evolution.Methods in molecular biology (Clifton, N.J.) · 2021Article
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Authors and funding
5 authors at 1 institution in 1 country.
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Abstract
The MYC protein is a transcription factor with oncogenic potential controlling fundamental cellular processes such as cell proliferation, metabolism, differentiation, and apoptosis. The MYC gene is a major cancer driver, and elevated MYC protein levels are a hallmark of most human cancers. We have previously shown that the brain acid-soluble protein 1 gene (BASP1) is specifically downregulated by the v-myc oncogene and that ectopic BASP1 expression inhibits v-myc-induced cell transformation. The 11-amino acid effector domain of the BASP1 protein interacts with the calcium sensor calmodulin (CaM) and is mainly responsible for this inhibitory function. We also reported recently that CaM interacts with all MYC variant proteins and that ectopic CaM increases the transactivation and transformation potential of the v-Myc protein. Here, we show that the presence of excess BASP1 or of a synthetic BASP1 effector domain peptide leads to displacement of v-Myc from CaM. The protein stability of v-Myc is decreased in cells co-expressing v-Myc and BASP1, which may account for the inhibition of v-Myc. Furthermore, suppression of v-Myc-triggered transcriptional activation and cell transformation is compensated by ectopic CaM, suggesting that BASP1-mediated withdrawal of CaM from v-Myc is a crucial event in the inhibition. In view of the tumor-suppressive role of BASP1 which was recently also reported for human cancer, small compounds or peptides based on the BASP1 effector domain could be used in drug development strategies aimed at tumors with high MYC expression.
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