ArticleScientific reports2014
Myeloid zinc finger 1 mediates sulindac sulfide-induced upregulation of death receptor 5 of human colon cancer cells.
Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- MZF1 Inhibits TGFβ-1/SMAD Signaling by Transcriptionally Activating SnoN to Augment Tumorigenic Potential in Colon Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Secretase promotes AD progression: simultaneously cleave Notch and APP.Frontiers in aging neuroscience · 2024Review
- The Roles of Zinc Finger Proteins in Colorectal Cancer.International journal of molecular sciences · 2023Review
- Review
- Tumor necrosis factor‑related apoptosis‑inducing ligand is a novel transcriptional target of runt‑related transcription factor 1.International journal of oncology · 2022Article
- Lestaurtinib potentiates TRAIL-induced apoptosis in glioma via CHOP-dependent DR5 induction.Journal of cellular and molecular medicine · 2020Article
- Review
- Therapeutic Targeting ofAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2019Article
- Sublytic C5b-9 induces proliferation of glomerular mesangial cells via ERK5/MZF1/RGC-32 axis activated by FBXO28-TRAF6 complex.Journal of cellular and molecular medicine · 2019Article
- MZF1 and SCAND1 Reciprocally RegulateCancers · 2019Article
- Role of the zinc finger and SCAN domain-containing transcription factors in cancer.American journal of cancer research · 2019Review
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Authors and funding
6 authors.
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Abstract
A combined therapy of sulindac sulfide and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a promising strategy for the treatment of cancer. Sulindac sulfide had been shown to induce the expression of death receptor 5 (DR5), a receptor for TRAIL, and sensitize cancer cells to TRAIL-induced apoptosis; however, the molecular mechanism underlying the upregulation of DR5 has not yet been elucidated. We demonstrate here that myeloid zinc finger 1 (MZF1) mediates the induction of DR5 by sulindac sulfide. Sulindac sulfide induced the expression of DR5 at the protein and mRNA levels in colon cancer SW480 cells. Furthermore, sulindac sulfide increased DR5 promoter activity. We showed that sulindac sulfide stimulated DR5 promoter activity via the -301 to -253 region. This region contained a putative MZF1-binding site. Site-directed mutations in the site abrogated the enhancement in DR5 promoter activity by sulindac sulfide. MZF1 directly bound to the putative MZF1-binding site of the DR5 promoter and the binding was increased by sulindac sulfide. The expression of MZF1 was also increased by sulindac sulfide, and MZF1 siRNA attenuated the upregulation of DR5 by sulindac sulfide. These results indicate that sulindac sulfide induces the expression of DR5 by up-regulating MZF1.
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