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Related Concept Videos

Cancer02:18

Cancer

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Cancers arise due to mutations in genes involved in the regulation of cell division, which leads to unrestricted cell proliferation. Modern science and medicine have made great strides in the understanding and treatment of cancer, including eradicating cancer in some patients. However, there is still no cure for cancer. This is largely due to the fact that cancer is a large group of many diseases.
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A Microfluidic Chip for the Versatile Chemical Analysis of Single Cells
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Microfluidic-based human prostate-cancer-on-chip.

Linan Jiang1, Hunain Khawaja2, Shekha Tahsin2

  • 1Department of Aerospace and Mechanical Engineering, Tucson, AZ, United States.

Frontiers in Bioengineering and Biotechnology
|February 7, 2024
PubMed
Summary
This summary is machine-generated.

A new Prostate-Cancer-on-Chip (PCoC) model recreates human prostate tumor and stroma interactions. This microfluidic system reveals how tumor cells induce cancer-associated fibroblasts (CAFs) and promote invasion, aiding prostate cancer research.

Keywords:
cancer-associated fibroblasts (CAFs)microfluidicsorgan-on-chipprostate cancerprostate tumor invasionstromal fibroblaststumor microenvironment

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Area of Science:

  • Biomedical Engineering
  • Cancer Biology
  • Microfluidics

Background:

  • Current prostate cancer models inadequately represent human physiology, hindering treatment development for therapy resistance and bone metastasis.
  • Existing in vitro models lack complexity, while in vivo animal models present physiological and genetic differences from humans.

Purpose of the Study:

  • To develop and validate the first in vitro microfluidic human Prostate-Cancer-on-Chip (PCoC) model.
  • To investigate dynamic tumor-stroma interactions, including cancer-associated fibroblast (CAF) conversion and tumor cell invasion.

Main Methods:

  • Co-cultivation of human prostate cancer and stromal fibroblast cells in a microfluidic device with a porous membrane.
  • Analysis of cell-cell signaling, CAF biomarker expression (αSMA, COL1A1), androgen receptor (AR) downregulation, and tumor invasion using immunofluorescence microscopy.
  • Simulation of solute concentration gradients to correlate with CAF conversion levels.

Main Results:

  • Prostate cancer cells induced CAF conversion in stromal fibroblasts, with conversion levels increasing along the medium flow direction.
  • Tumor cells downregulated stromal AR expression, unlike in normal prostate homeostasis.
  • The PCoC model demonstrated tumor cell and CAF invasion into neighboring compartments, highlighting the stroma's role in promoting metastasis.

Conclusions:

  • The developed PCoC model effectively recapitulates spatiotemporal tumor-stroma interactions and multicellular responses relevant to human prostate cancer in vivo.
  • This model serves as a valuable tool for dissecting prostate cancer mechanisms and exploring novel therapeutic strategies.