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Targeted Cancer Therapies

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The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
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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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Related Experiment Video

Updated: Jun 19, 2025

Quantifying Antibody-Dependent Cellular Cytotoxicity in a Tumor Spheroid Model: Application for Drug Discovery
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CD74-AKT Axis Is a Potential Therapeutic Target in Triple-Negative Breast Cancer.

Jingchao Wang1, Daoyuan Huang1, Thu Anh Thai Nguyen2

  • 1Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.

Biology
|July 26, 2024
PubMed
Summary

Triple-negative breast cancer cells resist apoptosis. Targeting CD74 and AKT pathways can restore this process, offering a new strategy for TNBC treatment.

Keywords:
AKTCD74FAS (CD95)apoptosischemoresistancepeptidomimetic drugtriple-negative breast cancer (TNBC)

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Triple-negative breast cancer (TNBC) exhibits resistance to apoptosis, a key mechanism for cancer cell death.
  • The role of CD74, a type II transmembrane protein, in cancer progression and chemoresistance is not fully understood.
  • Understanding the molecular mechanisms behind TNBC apoptosis resistance is crucial for developing effective therapies.

Purpose of the Study:

  • To investigate the role of CD74 in TNBC.
  • To elucidate the molecular mechanisms by which CD74 influences apoptosis resistance in TNBC.
  • To explore therapeutic strategies targeting the CD74 pathway for TNBC treatment.

Main Methods:

  • Gene expression analysis in cancer patients and patient-derived xenograft (PDX) models.
  • Assessment of CD74 expression correlation with cancer stem cell (CSC) and epithelial-mesenchymal transition (EMT) properties.
  • Investigation of the interaction between CD74, AKT signaling, and FAS-mediated apoptosis.
  • Evaluation of AKT inhibitors and CD74-derived peptides in restoring apoptosis.

Main Results:

  • CD74 is highly expressed in TNBC and correlates with CSC and EMT phenotypes.
  • AKT activation is critical for CD74 expression and stability, promoting oncogenic functions.
  • CD74 interacts with FAS, inhibiting FAS-mediated apoptosis.
  • Targeting the CD74/FAS and CD74-AKT axes synergistically restores apoptosis in TNBC cells.

Conclusions:

  • CD74 plays a significant role in promoting TNBC progression and apoptosis resistance.
  • The CD74/AKT axis is essential for maintaining CD74 expression and function in TNBC.
  • CD74 interferes with FAS-mediated apoptosis by directly binding to FAS.
  • Targeting the CD74/FAS and CD74-AKT pathways presents a promising therapeutic strategy for TNBC.