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Study Reveals Fat Tissue’s Role in Ovarian Cancer Spread

Fat cells, or adipose cells, 3D illustration

A recent study published in Nature Communications has uncovered significant insights into how the physical structure of fat tissue influences the spread of ovarian cancer. Conducted by researchers at Karolinska Institutet in Sweden and Queen Mary University of London, the research highlights that fat tissue not only provides chemical signals but also serves as a physical environment that facilitates cancer cell invasion.

The study reveals that ovarian cancer cells take advantage of the soft and densely packed structure of visceral fat to migrate swiftly and effectively throughout the body. This finding shifts the focus from purely biochemical factors to the mechanical properties of fat tissue, suggesting that the large size and deformability of fat cells create pathways—termed “migration highways”—for cancer cells. These pathways allow the cells to navigate through tight spaces while preserving their nuclei, a critical aspect for their survival and proliferation.

According to the lead author, Jordi Gonzalez Molina, a research specialist at the Department of Microbiology, Tumor and Cell Biology at both institutions, “Our study reveals how ovarian cancer cells exploit the unique physical properties of fat tissue to spread aggressively.” He noted that two primary factors contributing to these migration highways were the deformation of adipocytes caused by cancer cells and the size of these fat cells, both of which were linked to more aggressive tumors in patients.

Innovative Research Methodology

The research utilized advanced bioengineered models that replicate the characteristics of fat tissue, along with patient-derived samples. This innovative approach allowed the team to isolate and examine the effects of specific features, such as adipocyte size and tissue mechanics, on cancer cell movement.

Professor Kaisa Lehti, a researcher at the Department of Microbiology, Tumor and Cell Biology, emphasized the potential implications of this work. “Our newly engineered fat-mimicking platform opens doors to study other fat-linked cancers such as leukemia, breast cancer, and gastric cancer,” she stated. This research marks a pivotal shift in the focus of cancer treatment strategies, moving beyond the traditional methods of targeting cancer cells to also addressing their physical environments.

Future Directions and Collaborations

The research team plans to delve deeper into how other cell types, including fibroblasts and immune cells, interact with ovarian cancer cells during their invasion of fat tissue. They also aim to explore the mechanisms by which cancer cells induce fibrotic changes in fat tissue, a process that is known to contribute to therapy resistance.

This collaborative study brings together the expertise of Professor Kaisa Lehti and her team at Karolinska Institutet, as well as contributions from Professor Julien Gautrot at Queen Mary University of London. Special acknowledgments were made to the teams of Associate Professor Sahar Salehi and Assistant Professor Twana Alkasalias at Karolinska Institutet for their vital support in completing the research.

The findings of this study could not only enhance the understanding of ovarian cancer metastasis but also pave the way for new therapeutic strategies that target the mechanical aspects of tumor environments, potentially transforming the approach to treating cancers associated with fat tissue.

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