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Nature Is Weird  /  bioengineering

Colorectal cancer cells use the physical squeezing of your gut to turn themselves into more aggressive stem cells.

The KRAS G12C mutation makes individual cancer cells less viscous and much squishier than healthy ones. This decreased internal friction allows the cells to feel and react to the rhythmic contractions of your intestines. Standard medical models assume cancer spreads primarily through chemical signals, but these cells use mechanical force as fuel. Squeezing these mutated cells triggers a biological response that generates dangerous new cancer stem cells. This discovery means the physical environment of the digestive tract actively drives the progression of the disease. Controlling these mechanical forces could provide a completely new way to stop cancer from evolving.

Original Paper

Oncogene-Mechanics Axis: KRAS G12C Confers Agility Enabling Malignant Mechano-responses to Peristalsis in Colorectal Cancer

Lamichhane, A.; Cheburkanov, V.; Kizilov, M.; Shenoy, A.; Head, A. G.; Yakovlev, V.; Raghavan, S. A.

bioRxiv  ·  10.64898/2026.04.28.721453

Oncogene activity and mechanical forces individually and collectively drive colorectal cancer, yet the integration of these signals is unknown. We used a patented peristalsis bioreactor to determine how oncogenic KRAS G12C mutations alter the cellular response to colonic peristalsis. Although both healthy intestinal cells and KRAS G12C cancer cells sensed peristalsis via ERK phosphorylation, their mechano-responses diverged significantly. Peristalsis triggered a 9-fold enrichment of LGR5+ cancer