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Related Concept Videos

Negative Regulator Molecules01:23

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
Inhibition of Cdk Activity02:34

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The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
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Several proteins function as internal regulators to ensure each cell cycle stage is completed faithfully before proceeding to the next. Regulator molecules may act directly or influence the activity or production of other...

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[Corrigendum] Podoplanin‑mediated TGF‑β‑induced epithelial‑mesen‑ chymal transition and its correlation with bHLH transcription factor DEC in TE‑11 cells.

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Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay
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Published on: May 3, 2018

Basic helix-loop-helix transcription factor DEC1 negatively regulates cyclin D1.

Ujjal K Bhawal1, Fuyuki Sato, Yuki Arakawa

  • 1Research Institute of Occlusion Medicine and Open Research Center, Kanagawa Dental College, Yokosuka, Japan. bhawal.ujjal.kumar@nihon-u.ac.jp

The Journal of Pathology
|April 21, 2011
PubMed
Summary

DEC1, a transcriptional regulator, delays wound healing and reduces cancer cell invasion by repressing cyclin D1. DEC1 also activates the PI-3K/Akt pathway, impacting cancer progression.

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Area of Science:

  • Molecular Biology
  • Cancer Research
  • Circadian Rhythms

Background:

  • DEC1 and DEC2 are paralogous bHLH transcriptional regulators with circadian expression patterns.
  • DEC1 is implicated in cell differentiation, cell cycle, circadian regulation, hypoxia response, and carcinogenesis.

Purpose of the Study:

  • To investigate the role of DEC1 in cell proliferation, migration, invasion, and its relationship with cyclin D1 in oral cancer.
  • To elucidate the signaling pathways involved in DEC1-mediated effects, including PI-3K/Akt signaling.

Main Methods:

  • Overexpression of DEC1 in cellular models.
  • Reporter assays to assess promoter activity (cyclin D1).
  • Analysis of DEC1 binding to the cyclin D1 promoter.
  • Correlation analysis of DEC1 and cyclin D1 expression in clinical oral cancer samples.
  • Investigation of PI-3K/Akt signaling pathway activation.

Main Results:

  • DEC1 overexpression delayed wound healing and reduced cell proliferation, migration, and invasion.
  • DEC1 directly repressed cyclin D1 promoter activity and expression.
  • A strong inverse correlation between DEC1 and cyclin D1 expression was observed in oral cancer.
  • DEC1 expression correlated significantly with clinicopathological parameters.
  • DEC1 overexpression activated the PI-3K/Akt signaling pathway via ROS.

Conclusions:

  • DEC1 plays a significant role in inhibiting cancer cell proliferation, migration, and invasion, partly through repression of cyclin D1.
  • DEC1 expression is inversely correlated with cyclin D1 in oral cancer and associated with clinicopathological features.
  • DEC1 activates the PI-3K/Akt pathway, suggesting a complex role in cancer progression and response to radiation.