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  1. Home
  3. Lymphatic Invasion Of Plakoglobin-dependent Tumor Cell Clusters Drives Formation Of Polyclonal Lung Metastases In Colon Cancer.
  1. Home
  3. Lymphatic Invasion Of Plakoglobin-dependent Tumor Cell Clusters Drives Formation Of Polyclonal Lung Metastases In Colon Cancer.

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Lymphatic Invasion of Plakoglobin-Dependent Tumor Cell Clusters Drives Formation of Polyclonal Lung Metastases in

Emre Küçükköse1, Jamila Laoukili1, Alexander N Gorelick2

  • 1Division of Imaging and Cancer, Laboratory of Translational Oncology, University Medical Center Utrecht, Utrecht, The Netherlands.

Gastroenterology
|March 11, 2023

View abstract on PubMed

Summary
This summary is machine-generated.

Colon cancer lung metastasis is distinct from liver metastasis. It involves tumor cell clusters, not single cells, and relies on plakoglobin and lymphatic vessels for spread.

Keywords:
LymphaticsMetastasis MechanismOrgan TropismPatient-Derived Organoids

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Area of Science:

  • Oncology
  • Cancer Metastasis Research
  • Molecular Biology

Background:

  • Colon cancer liver metastases are surgically curable, but lung metastases complicate treatment.
  • Mechanisms driving lung metastasis in colon cancer remain poorly understood.

Purpose of the Study:

  • To elucidate the distinct mechanisms governing lung versus liver metastasis formation in colon cancer.
  • To identify key molecular determinants and cellular processes involved in lung metastasis.

Main Methods:

  • Established patient-derived organoid (PDO) cultures from colon tumors with varied metastatic patterns.
  • Developed mouse models by implanting PDOs, using optical barcoding to trace metastasis origins.
  • Employed RNA sequencing, immunohistochemistry, and genetic/pharmacologic manipulations for mechanistic insights.

Main Results:

  • Distinct metastatic organotropism (liver only, lung only, liver and lung) was observed in PDO models.
  • Liver metastases originated from single cells, while lung metastases arose from polyclonal clusters via lymphatic vasculature.
  • High plakoglobin expression correlated with lung metastasis, driving tumor cell cluster formation and lymphatic invasion.

Conclusions:

  • Lung and liver metastasis formation are fundamentally different processes with distinct bottlenecks and seeding mechanisms.
  • Polyclonal lung metastases depend on plakoglobin-mediated tumor cell clusters entering the lymphatic system.
  • Targeting lymphangiogenesis and plakoglobin may offer therapeutic strategies for lung metastasis.