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The immersion of cancer cells and subsequent metastasis are the leading causes of death in patients.
Malignancies in the brain, including glioblastoma (GBM), are characterized by a high invasive ability to cause tumors to spread in the brain, a pattern of cell growth that is largely due to the failure of current treatment strategies and poor prognosis in patients.
glioblastoma (GBM) as the most aggressive primary brain tumor, its immersion seriously hinders surgical excision treatment, and reduces the effectiveness of systemic therapy due to the relationship between the blood and brain barrier.
because of the special structure of the adult brain, GBM aggression is different from the classic blood vessels or lymphatic pathways associated with peripheral metastatic cancer.
Although there is some understanding of the mechanisms of GBM cell invasion (e.g. cytostebrae remodeling, protease secretion, in-cell signal transductivity), the development of treatments for GBM invasion and the search for new targets to regulate the cell invasion process are particularly important.
the expression level of ZFAND3 was associated with GBM cell invasion In this study, the researchers used genome-wide interference screening techniques to identify genes associated with cell invasion and determined that ZFAND3 was a key driver of GBM aggression.
in patient-derived cell models, the researchers found that the absence of ZFAND3 hindered GBM's ability to attack, while over-expression of ZFAND3 increased the motor ability of initially non-invasive cells.
mechanism studies show that the activity of ZFAND3 requires its nuclear positioning and complete zinc finger domain.
further studies have shown that ZFAND3 plays a key role in nuclear protein complexes, activating gene transcription and regulating the initiation of cell invasion-related genes, including COL6A2, FN1, and NRCAM.
and the function of ZFAND3 in GBM and other immersive cancers needs further study.
of ZFAND3's model diagram for cell invasion, the results reveal that ZFAND3 is a transcriptional regulator of cell invasion-related genes that enhances the immersion of GBM cells.
can be a potential treatment strategy for GBM by targeting the activity of ZFAND3.
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