Fam111b identified as an important driver of glioma progression and therapeutic target

Fam111b identified as an important driver of glioma progression and therapeutic target

Gliomas are among the deadliest brain tumors with limited treatment options and poor survival rates. Scientists from China identified FAM111B, a DNA repair-associated protein, as a key driver of glioma progression. The study shows that overexpression of FAM111B improves tumor growth and aggressiveness through activation of the PI3K/AKT pathway. This is the first research linking FAM111b to gliomas, providing a promising new biomarker and therapeutic target for this intractable disease.

Gliomas are the most common and aggressive form of primary brain tumors in adults, with dismal survival rates despite surgery, radiation and chemotherapy. Scientists continue to search for molecular drivers that could serve as new therapeutic targets. Now researchers led by Dr. Quan DU from Zhejiang Chinese Medical University and Westlake University in China identified a promising candidate: a protein called FAM111B.

“Our results showed that FAM111B influenced glioma malignancy by modulating the PI3K/AKT pathway“Highlights from leading researcher Dr. Du.”This provides a new potential opportunity for therapeutic interventions in the treatment of glioma.“

The study published on May 19, 2025 in theChinese neurosurgical journalis the first to investigate the role of FAM111b in gliomas. Previous studies had linked FAM111B to cell cycle regulation, DNA repair and fibrosis-related diseases. However, its function in brain cancer was previously unknown.

Using genomic databases, including the Cancer Genome Atlas (TCGA) and the Chinese Glioma Genome Atlas (CGGA), the research team found significantly elevated levels in glioma tissue compared to healthy brain tissue. In addition, higher expression levels correlated with older patient age, more advanced tumor grade, and worse clinical outcomes - including reduced overall survival and disease-free survival. The authors confirmed these results experimentally. Glioma cell lines and tumor samples showed significantly higher levels of FAM111B protein compared to normal tissues. When Fam111b was overexpressed in glioma cells, their proliferation, invasion, and migration increased dramatically. Conversely, knocking FAM111B suppressed these malignant features.

Furtherin vivoExperiments in mice confirmed the role of FAM111B in promoting tumor growth. Mice with glioma cells overexpressing FAM111b developed significantly larger and heavier tumors than controls.
To uncover the molecular mechanism behind these effects, the team performed pathway enrichment analysis. The results strongly implicated the PI3K/Akt signaling cascade – a pathway long linked to tumor growth and resistance to therapy. Further testing showed that overexpression of FAM111B increased phosphorylation of PI3K and AKT, while silencing the protein had the opposite effect.

“Fam111b regulates the malignant characteristics of glioma cells via the PI3K/AKT pathway“The Dr. Du wrote.”These results support the hypothesis that FAM111b influences the malignant characteristics of glioma cells mainly through the PI3K/Akt pathway. The limitations of the study, particularly the small patient size and the need for broader validation in multiple research centers.
However, the effects are significant. Identifying FAM111B as an independent prognostic marker and a key modulator of a known cancer pathway adds a valuable tool to the glioma research arsenal.

While therapies targeting the PI3K/AKT pathway already exist, this research may pave the way for more precise, fam111b-guided interventions. “Fam111b is not only considered a critical biomarker for the development of glioma"Dr. you're closing,"but also as a promising novel target for therapeutic interventions. “

As researchers work to solve the complex puzzle of brain cancer, FAM111B may soon take center stage.

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