Data from Cancer-Associated Fibroblasts Induce a Collagen Cross-link Switch in Tumor Stroma Article Swipe

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Daniela Paňková , Yulong Chen , Masahiko Terajima , Mark J. Schliekelman , Brandi N. Baird , Monica Fahrenholtz , Sun Li , Bartley J. Gill , Tegy J. Vadakkan , Min P. Kim , Young‐Ho Ahn , Jonathon D. Roybal , Xin Liu , Edwin R. Parra , Jaime Rodrı́guez , Ignacio I. Wistuba , Chad J. Creighton , Don L. Gibbons , John M. Hicks , Mary E. Dickinson , Jennifer West , K. Jane Grande‐Allen , Samir Hanash , Mitsuo Yamauchi , Jonathan M. Kurie ·

YOU? · · 2023 · Open Access · · DOI: https://doi.org/10.1158/1541-7786.c.6540138.v1

Intratumoral collagen cross-links heighten stromal stiffness and stimulate tumor cell invasion, but it is unclear how collagen cross-linking is regulated in epithelial tumors. To address this question, we used Kras^LA1 mice, which develop lung adenocarcinomas from somatic activation of a Kras^G12D allele. The lung tumors in Kras^LA1 mice were highly fibrotic and contained cancer-associated fibroblasts (CAF) that produced collagen and generated stiffness in collagen gels. In xenograft tumors generated by injection of wild-type mice with lung adenocarcinoma cells alone or in combination with CAFs, the total concentration of collagen cross-links was the same in tumors generated with or without CAFs, but coinjected tumors had higher hydroxylysine aldehyde–derived collagen cross-links (HLCC) and lower lysine-aldehyde–derived collagen cross-links (LCCs). Therefore, we postulated that an LCC-to-HLCC switch induced by CAFs promotes the migratory and invasive properties of lung adenocarcinoma cells. To test this hypothesis, we created coculture models in which CAFs are positioned interstitially or peripherally in tumor cell aggregates, mimicking distinct spatial orientations of CAFs in human lung cancer. In both contexts, CAFs enhanced the invasive properties of tumor cells in three-dimensional (3D) collagen gels. Tumor cell aggregates that attached to CAF networks on a Matrigel surface dissociated and migrated on the networks. Lysyl hydroxylase 2 (PLOD2/LH2), which drives HLCC formation, was expressed in CAFs, and LH2 depletion abrogated the ability of CAFs to promote tumor cell invasion and migration.Implications: CAFs induce a collagen cross-link switch in tumor stroma to influence the invasive properties of tumor cells. Mol Cancer Res; 14(3); 287–95. ©2015 AACR.

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Cancer-Associated Fibroblasts KRAS Cancer research Chemistry Adenocarcinoma Lysyl oxidase Stromal cell Lung cancer Type I collagen Tumor microenvironment Stroma Cell Pathology Molecular biology Cancer Biology Colorectal cancer Extracellular matrix Medicine Internal medicine Biochemistry Tumor cells Immunohistochemistry

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Type: preprint
Language: en
Landing Page: https://doi.org/10.1158/1541-7786.c.6540138.v1
OA Status: gold
Related Works: 10
OpenAlex ID: https://openalex.org/W4362493392

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DOI: https://doi.org/10.1158/1541-7786.c.6540138.v1

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Title: Data from Cancer-Associated Fibroblasts Induce a Collagen Cross-link Switch in Tumor Stroma

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Language: en

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Publication year: 2023

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Publication date: 2023-04-03

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Authors: Daniela Paňková, Yulong Chen, Masahiko Terajima, Mark J. Schliekelman, Brandi N. Baird, Monica Fahrenholtz, Sun Li, Bartley J. Gill, Tegy J. Vadakkan, Min P. Kim, Young‐Ho Ahn, Jonathon D. Roybal, Xin Liu, Edwin R. Parra, Jaime Rodrı́guez, Ignacio I. Wistuba, Chad J. Creighton, Don L. Gibbons, John M. Hicks, Mary E. Dickinson, Jennifer West, K. Jane Grande‐Allen, Samir Hanash, Mitsuo Yamauchi, Jonathan M. Kurie

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Concepts: Cancer-Associated Fibroblasts, KRAS, Cancer research, Chemistry, Adenocarcinoma, Lysyl oxidase, Stromal cell, Lung cancer, Type I collagen, Tumor microenvironment, Stroma, Cell, Pathology, Molecular biology, Cancer, Biology, Colorectal cancer, Extracellular matrix, Medicine, Internal medicine, Biochemistry, Tumor cells, Immunohistochemistry

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