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Related Concept Videos

Overview of Exosomes01:36

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Exosomes are stable, lipid bilayer-enclosed vesicles capable of crossing biological barriers. They can carry a wide range of molecules required for intercellular communication. Once exosomes are released from the cell where they originated, they enter a recipient cell through various pathways such as fusion, receptor-mediated endocytosis, macropinocytosis, and phagocytosis.
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Related Experiment Video

Updated: May 27, 2025

Detection of a Circulating MicroRNA Custom Panel in Patients with Metastatic Colorectal Cancer
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Low miR-224-5p in exosomes confers colorectal cancer 5-FU resistance by upregulating S100A4.

Yan-Yan Yan1, Zhuo-Fen Deng2, Xing-Tao Wu2

  • 1Guangzhou Municipal and Guangdong Provincial Key Laboratory of Molecular Target & Clinical Pharmacology, the NMPA and State Key Laboratory of Respiratory Disease, School of Pharmaceutical Sciences and the Fifth Affiliated Hospital, Guangzhou Medical University, Guangzhou 511436, PR China; Institute of Immunology, School of Medicine, Shanxi Datong University, Datong 037009, PR China.

Drug Resistance Updates : Reviews and Commentaries in Antimicrobial and Anticancer Chemotherapy
|February 16, 2025
PubMed
Summary
This summary is machine-generated.

This study identifies miR-224-5p as a key regulator in colorectal cancer (CRC) 5-fluorouracil (5-FU) resistance, targeting S100A4. Lower miR-224-5p levels correlate with poorer prognosis and 5-FU resistance in CRC patients.

Keywords:
5-Fluorouracil (5-FU) resistanceColorectal cancer (CRC)ExosomeMiR-224–5pS100A4Triptolide (TPL)Verapamil

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Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • 5-fluorouracil (5-FU) is a cornerstone chemotherapy for colorectal cancer (CRC).
  • Acquired resistance to 5-FU significantly limits treatment efficacy in CRC patients.
  • Identifying molecular mechanisms underlying 5-FU resistance is crucial for developing effective therapeutic strategies.

Purpose of the Study:

  • To elucidate molecular markers mediating 5-fluorouracil (5-FU) resistance in colorectal cancer (CRC).
  • To investigate the role of miR-224-5p and S100A4 in 5-FU resistance and CRC progression.
  • To explore potential therapeutic interventions targeting the identified molecular pathway.

Main Methods:

  • Exosome isolation and characterization from 5-FU resistant CRC cells (HCT-15/FU).
  • miRNA sequencing (miR-Seq) and proteomic analysis of CRC cells and patient serum exosomes.
  • In vitro and in vivo functional assays to assess the role of miR-224-5p and S100A4.
  • Bioinformatic analysis of public CRC patient databases.
  • Drug sensitivity assays with 5-FU, verapamil, and triptolide.

Main Results:

  • Exosomes from 5-FU resistant CRC cells promoted 5-FU resistance and malignancy in recipient cells.
  • miR-224-5p was significantly downregulated, and S100 calcium-binding protein A4 (S100A4) was upregulated in 5-FU resistant CRC cells and patients.
  • Lower miR-224-5p and higher S100A4 expression correlated with poorer prognosis in CRC patients.
  • miR-224-5p directly targets S100A4, and this axis regulates 5-FU resistance and CRC cell malignancy.
  • Combination therapy with 5-FU and verapamil (a calcium antagonist) or triptolide reversed 5-FU resistance by modulating the miR-224-5p/S100A4 pathway.

Conclusions:

  • miR-224-5p acts as a tumor suppressor by downregulating S100A4, playing a critical role in CRC 5-FU resistance.
  • miR-224-5p may serve as a predictive biomarker for 5-FU resistance in CRC.
  • Targeting the miR-224-5p/S100A4 pathway with agents like verapamil or triptolide offers potential therapeutic strategies for 5-FU resistant CRC.