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Related Concept Videos

Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

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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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Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
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Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
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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.
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Disrupting Cell Cycle Machinery: CREPT Is an Emerging Target in Cancer Therapy.

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Cell-cycle-related and expression-elevated protein in tumors (CREPT) drives cancer by activating key pathways. Targeting CREPT shows promise for reversing tumor growth and enhancing immunotherapies.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Cell-cycle-related and expression-elevated protein in tumors (CREPT) is a transcriptional co-factor.
  • CREPT dysregulation drives tumorigenesis by activating oncogenic signaling pathways like Wnt/β-catenin, STAT3, and NF-κB/TNFR2.
  • Aberrant CREPT expression correlates with poor patient survival across various cancers.

Purpose of the Study:

  • To review the multifaceted roles of CREPT in cancer.
  • To explore CREPT's involvement in the hallmarks of cancer.
  • To propose CREPT as a therapeutic target for cancer treatment.

Main Methods:

  • Review of preclinical studies involving CREPT knockdown using shRNA.
  • Analysis of research on CREPT's functions in metabolic regulation, tissue repair, and microenvironmental remodeling.
  • Examination of current strategies targeting CREPT, including miRNA-based approaches.

Main Results:

  • CREPT knockdown demonstrated sustained tumor growth regression in preclinical models.
  • CREPT regulates multiple cancer-promoting signaling pathways.
  • Emerging evidence highlights CREPT's pleiotropic functions beyond cell cycle control.

Conclusions:

  • Targeting CREPT holds significant potential to reverse tumor progression.
  • Combining CREPT inhibition with immune checkpoint inhibitors may improve efficacy in CREPT-driven cancers.
  • Further research into direct CREPT inhibitors is warranted for clinical application.