Researchers from the University of Illinois Urbana-Champaign have discovered a protein that can predict which breast cancer patients will respond well to chemotherapy and immunotherapy. After conducting genome-wide screening in human cancer cells, the research team found that the FGD3 protein was a promising biomarker in determining chemotherapy and immunotherapy efficacy.
Patients with high FGD3 levels responded favorably to treatment across all breast cancer types, while those with low levels show poor responses, Professor of biochemistry David J. Shapiro notes.
The findings build on 2021 research when the team developed ErSO, an experimental drug that killed 100 percent of breast cancer cells in mice including metastases without major side effects. ErSO works by binding to estrogen receptors and overactivating a cellular pathway that shields cancer cells during rapid growth. By up-regulating this pathway, the researchers found that they could trigger a process called lytic cell death wherein cells literally swell and rupture.
According to Shapiro, most cancer drugs work by blocking something cells need to survive, either inhibiting cancer cells growth or, in some cases, causing programmed cell death or apoptosis. ErSO does the opposite by cranking up cellular machinery until cancer cells burst open.
The research team wanted to understand how this mechanism worked at the molecular level to make ErSO so effective. Using genome-wide CRISPR screening, the researchers identified FGD3, a little-studied protein whose function remained unclear despite being linked to favorable breast cancer outcomes, as the top candidate.
Experiments manipulating FGD3 levels confirmed that the protein controls whether ErSO can kill cancer cells by weakening cellular architecture and making swollen cancer cells more likely to rupture. When the cells burst, the molecules they release trigger immune system responses that in turn recruit macrophages and natural killer cells to attack tumors.
Furthermore, FGD3 reorganizes the actin filaments responsible for providing cellular structure, essentially weakening the structure and encouraging membrane rupture.
Human cell experiments and patient-derived organoids demonstrated FGD3’s necessity for the rupture process. Mouse studies showed higher FGD3 levels enhanced anticancer effects not only for ErSO but also for standard chemotherapy drugs such as doxorubicin and epirubicin. Patient data analysis revealed similar patterns, with better prognosis and chemotherapy treatment response correlating with higher FGD3 levels.
Additionally, the protein dramatically increases movement of another molecule to cancer cell surfaces that stimulates natural killer cells to target tumors for destruction, Shapiro says. He notes that this mechanism could enhance immunotherapy effectiveness while reducing toxic drug doses needed for treatment. The potential proves particularly important for breast cancer, where immunotherapy has shown limited success against solid tumors compared to other cancer types.
This correlation between FGD3 levels and treatment response appears to be consistent across all breast cancer subtypes and chemotherapy types tested. Further studies will explore whether other types of tumors and cancer treatment approaches could have a similar reaction to FGD3.
For companies like Calidi Biotherapeutics Inc. (NYSE American: CLDI) that are focused on developing new immunotherapies targeting different kinds of cancer, any new information shedding additional light on how different structures within human cells work to counter or bolster disease progression is welcome. This is because such information broadens the range of mechanisms that can be leveraged in the fight against cancer.
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