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Related Experiment Video

Updated: Feb 14, 2026

Monitoring Breast Cancer Growth and Metastatic Colony Formation in Mice using Bioluminescence
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Novel Cell Cycle Inhibitors Decrease Primary and Metastatic Breast Cancer Growth In Vivo.

Mir Shahid Maqbool1, Yongzhan Zhang2, Karin Strittmatter2

  • 1Division of Cancer Pharmacology, CSIR-Indian Institute of Integrative Medicine, Sanat Nagar, Srinagar 190005, Jammu & Kashmir, India.

Cancers
|February 13, 2026
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Summary

Researchers identified five novel meriolin derivatives that inhibit cyclin-dependent kinases (CDKs) and show promise in treating metastatic breast cancer by reducing tumor growth and spread.

Keywords:
breast cancercirculating tumor cellsdrug screenmouse model

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Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Breast cancer metastasis is a major cause of mortality, necessitating new therapeutic strategies.
  • Existing treatments for metastatic breast cancer are limited, highlighting the need for innovative approaches.

Purpose of the Study:

  • To identify novel small-molecule compounds for treating metastatic breast cancer.
  • To evaluate the efficacy and mechanisms of action of identified compounds.

Main Methods:

  • Conducted a small-molecule drug screen using patient-derived circulating tumor cells (CTCs).
  • Utilized high-content imaging microscopy to assess compound efficacy in vitro and in vivo.
  • Performed bulk RNA sequencing and Gene Ontology analysis to understand molecular mechanisms.

Main Results:

  • Identified five meriolin derivatives with cyclin-dependent kinase (CDK-2/9) inhibitory activity.
  • Validated compound efficacy in inhibiting cell cycle, tumor growth, and metastasis in mouse models.
  • Transcriptome profiling revealed cell cycle regulation pathway alterations.

Conclusions:

  • The identified meriolin derivatives are promising candidates for breast cancer treatment.
  • Integrated drug screening, transcriptomics, and in vivo validation offer a robust approach for drug discovery.