Mon Sep 09 14:18:32 UTC 2024: ## Tiny Glitch in Human Genes May Contribute to Cancer Susceptibility
**Bangalore, India** – A new study from the Indian Institute of Science has uncovered a potential link between a genetic quirk unique to humans and chimpanzees and increased susceptibility to cancer. The research, published in the *Journal of Cell Science*, reveals that a specific gene, FEM1B, exhibits a “stop codon readthrough” phenomenon, leading to the production of a longer, unstable version of the protein it encodes.
This unusual process is triggered by a single nucleotide insertion that occurred approximately 10 million years ago, just as humans and chimpanzees diverged from other primates. The resulting longer FEM1B protein is then marked for degradation, leading to reduced levels of the protein in the cell.
The FEM1B protein plays a vital role in regulating cell division. It acts as a tag for other proteins, marking them for destruction. By controlling the levels of these targeted proteins, FEM1B helps ensure proper cell cycle progression and prevents uncontrolled cell growth, a hallmark of cancer.
The research team, led by Associate Professor Sandeep Eswarappa, demonstrated that preventing this stop codon readthrough in cancer cell lines resulted in increased levels of the FEM1B protein. This, in turn, led to enhanced degradation of its target proteins, slowing down the cell cycle and ultimately inhibiting tumor growth in mice models.
Furthermore, analysis of human cancer patient data revealed a correlation between higher FEM1B gene expression and increased survival rates, supporting the study’s hypothesis.
The discovery sheds light on a potential evolutionary factor contributing to human cancer vulnerability. The researchers speculate that this single nucleotide insertion, while seemingly minor, may have contributed to the increased cancer susceptibility observed in humans compared to other primates.
However, the exact mechanism behind this stop codon readthrough remains a mystery. The team is currently investigating the molecular machinery involved in this process, hoping to identify potential therapeutic targets to manipulate the readthrough and control tumor progression.
This groundbreaking research offers valuable insights into the complex interplay between evolution, genetics, and cancer. It provides a new avenue for exploration in developing novel cancer therapies by potentially targeting this unique genetic glitch in humans.
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