This genetic alteration may explain why humans are more susceptible to cancer compared to other primates.

A recent study published in the Journal of Cell Science investigates the FEM1B gene, revealing that its mRNA readthrough significantly influences the cell cycle and has implications for cancer cell proliferation.

The study highlights a phenomenon known as stop codon readthrough, where the protein synthesis machinery occasionally skips the stop codon, resulting in longer proteins.

Evolutionary analysis suggests that the stop codon readthrough process is unique to humans and chimpanzees, potentially linked to a single nucleotide insertion that occurred around 10 million years ago.

Sandeep Eswarappa, an Associate Professor at the Indian Institute of Science, notes that such readthrough can affect a protein's localization, stability, and function.

The FEM1B protein plays a crucial role in marking other proteins for degradation, thereby regulating various cellular processes, including the cell cycle.

Researchers discovered that stop codon readthrough produces a longer and more unstable version of FEM1B, which ironically leads to its degradation and reduced protein levels.

Using CRISPR-Cas9 technology, the research team eliminated the sequence responsible for readthrough in cancer cell lines, resulting in increased FEM1B levels, enhanced degradation of target proteins, and a delayed cell cycle, ultimately reducing cancer cell proliferation.

In mouse models, cancer cell lines that lacked readthrough exhibited slower tumor growth.

The research team is focused on uncovering the molecular mechanisms behind stop codon readthrough to develop targeted therapeutic strategies aimed at controlling tumor progression.

Analysis of data from human cancer patients showed that higher expression levels of the FEM1B gene correlate with better survival rates, supporting the study's findings.

Protein synthesis, or translation, involves assembling amino acids based on genetic information from mRNA, which is read in groups of three called codons.