Friction is a force we experience every day, often without realizing it. It is the resistance that occurs when two surfaces move or try to move against each other. Thanks to friction, we can walk without slipping, write with a pen, and hold objects firmly in our hands. Without it, even simple activities would become extremely difficult.
One of the most significant impacts of cellular plasticity in colorectal cancer is therapy resistance. When exposed to chemotherapy or targeted treatments, some cancer cells can change their characteristics, temporarily entering a dormant or stem-like state. These adaptable cells often survive treatment and later re-emerge, leading to tumor relapse and disease progression.
Cellular plasticity is also closely linked to cancer stem cells, a small but powerful population within colorectal tumors. These cells possess self-renewal capabilities and can generate diverse cancer cell types. Plasticity allows non-stem cancer cells to revert into stem-like cells, increasing tumor heterogeneity and making the cancer harder to eliminate completely.
The tumor microenvironment further fuels cellular plasticity in colorectal cancer. Signals from surrounding immune cells, fibroblasts, and inflammatory factors can push cancer cells to change their behavior. This dynamic interaction enables cancer cells to invade nearby tissues and spread to distant organs, contributing to metastasis.
Understanding cellular plasticity opens new opportunities for colorectal cancer treatment. Instead of targeting only specific cancer cell types, future therapies may aim to block the mechanisms that allow cells to switch identities. By limiting plasticity, it may be possible to prevent tumor growth, reduce resistance, and improve long-term outcomes for patients.
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