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Reprogrammed Schwann Cells Organize into Dynamic Tracks that Promote Pancreatic Cancer Invasion.

Sylvie Deborde^1,2, Laxmi Gusain¹, Ann Powers¹

¹Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, New York.

Cancer Discovery

|July 26, 2022

Summary

This summary is machine-generated.

Schwann cells (SC) activated by cancer form tumor-activated Schwann cell tracks (TAST) that promote pancreatic cancer invasion. This study reveals SCs exploit nerve repair pathways to enhance cancer cell motility and spread.

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Area of Science:

Oncology
Neuroscience
Cancer Biology

Background:

Nerves are part of the tumor microenvironment, influencing cancer progression.
The specific role of nerve cells in cancer invasion is not fully understood.

Purpose of the Study:

To investigate how Schwann cells (SCs) contribute to cancer cell migration and invasion.
To elucidate the mechanism by which SCs facilitate cancer spread within the tumor microenvironment.

Main Methods:

Analysis of Schwann cell gene expression signatures in pancreatic ductal adenocarcinoma.
Observation of dynamic Schwann cell track formation and force application on cancer cells.
Investigation of c-Jun activation in Schwann cells during cancer invasion.

Main Results:

Activated Schwann cells form tumor-activated Schwann cell tracks (TASTs) that promote cancer cell migration and invasion.
Nonmyelinating SCs in TASTs correlate with reduced patient survival in pancreatic cancer.
Schwann cells utilize c-Jun activation, similar to nerve repair, to organize into tracks and enhance cancer cell motility.

Conclusions:

Schwann cells, activated by cancer, form tracks that serve as pathways for cancer invasion.
Cancer cells co-opt the wound repair process involving Schwann cells to facilitate their spread.
This mechanism offers novel therapeutic targets for inhibiting cancer metastasis.