ArticleOncotarget2017
TSC-22 inhibits CSF-1R function and induces apoptosis in cervical cancer.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Novel Insights into TSC22D Family Genes in Metabolic Diseases and Cancer.Biomolecules · 2026Review
- TSC22D1 is a newly identified inhibitor of insulin secretion in pancreatic beta cells.The FEBS journal · 2025Article
- Pharmacologic inhibition of CSF-1R suppresses intrinsic tumor cell growth in osteosarcoma with CSF-1R overexpression.Journal of translational medicine · 2025Article
- CSF-1R in Cancer: More than a Myeloid Cell Receptor.Cancers · 2024Review
- Transforming Stimulated Clone 22 (TSC-22) Interacts Directly with Bromodomain-Containing Protein 7 (BRD7) to Enhance the Inhibition of Extracellular Signal-Regulate Kinase (ERK) Pathway in Ovarian Cancer.Development & reproduction · 2022Article
- Article
- Identification of Binding Proteins for TSC22D1 Family Proteins Using Mass Spectrometry.International journal of molecular sciences · 2021Article
- RUNX-1 haploinsufficiency causes a marked deficiency of megakaryocyte-biased hematopoietic progenitor cells.Blood · 2021Article
- Increased invasive phenotype of CSF-1R expression in glioma cells via the ERK1/2 signaling pathway.Cancer gene therapy · 2019Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colony stimulating factor 1 receptor (CSF-1R) regulates the monocyte/macrophage system, which is an essential component of cancer development. Therefore, CSF-1R might be an effective target for anti-cancer therapy. The overexpression of transforming growth factor (TGF)-β stimulated clone-22 (TSC-22) inhibits cancer cell proliferation and induces apoptosis, and TSC-22 is emerging as a key factor in tumorigenesis. In this study, we discovered CSF-1R as a new interacting partner of TSC-22 and identified its elevated expression in cervical cancer cells. In particular, we found that TSC-22 interacted with the intracellular tyrosine kinase insert domain (539-749) of CSF-1R, which activates the AKT and ERK signaling pathways. This binding blocked AKT and ERK signaling, thereby suppressing the transcriptional activity of NF-κB. The overexpression of TSC-22 significantly decreased CSF-1R protein levels, affecting their autocrine loop. TSC-22 injected into a xenograft mouse model of human cervical cancer markedly inhibited tumor growth. The reduction of CSF-1R protein significantly suppresses cervical cancer cell proliferation and motility and induces apoptotic cell death. This association between TSC-22 and CSF-1R could be used as a novel therapeutic target and prognostic marker for cervical cancer.
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