FERMT1 (Fermitin Family Member 1)

Functional assays demonstrated that FERMT1 deletion reduced LUAD cell migration and invasion. FERMT1 serves as a potential biomarker for LUAD prognosis and cancer immunotherapy, highlighting its role in tumor progression and therapeutic response.

This study highlights the power of NGS in diagnosing genetically distinct disorders without shared pathogenic mechanisms within a single family. Our findings underscore the clinical value of comprehensive genomic sequencing for unravelling complex hereditary conditions, especially when multiple rare disorders segregate independently in kindreds.

Using gain and loss-of-function experiments, we demonstrate that FERMT1 overexpression protects glioma cells from erastin-induced ferroptosis, while FERMT1 deficiency sensitizes cells to ferroptotic cell death...Collectively, our findings reveal a previously unrecognized FERMT1-MBOAT2 axis that regulates ferroptosis in glioma cells and provide new insights into the molecular mechanisms underlying glioma progression. Targeting this axis may offer a novel therapeutic strategy for inducing ferroptosis and improving treatment outcomes in glioma.

Young women's tumors exhibited lower estrogen receptor (ER) expression yet paradoxically enhanced ER response pathways and increased expression of tamoxifen-resistance-associated genes (IRS1, FERMT1)...Finally, differential expression of four immune-related surface proteins also suggested the potential of age-specific responses to immune-based therapies. Together, these findings may contribute to the understanding of the molecular mechanisms underlying worse outcomes in young women and offer new insight to therapeutic strategies.

Significantly, FERMT2 silencing reduced the directional migration in all three cell types. These findings are consistent with the concept that, in the absence of other Kindlin orthologues, Kindlin-2 plays a prominent role in the modulation of the proliferation, spreading, focal adhesion assembly, and motility of transformed keratinocytes, as exemplified by PM1 and MET4 cells.

Our study demonstrates that Kindlin-1 significantly influences HCC progression by regulating mitophagy through the PINK1/Parkin pathway. Inhibiting Kindlin-1 may represent a promising therapeutic strategy to enhance the efficacy of donafenib, thereby providing novel insights into improving treatment outcomes for HCC patients.

Additionally, qPCR experiments validated the expression of these genes in pancreatic cancer cell lines. These results offer valuable insights into PC progression, providing a foundation for improved clinical management and future research.

The patient's phenotype is likely caused by the resulting truncated and non-functioning protein. Our report further enriches the spectrum of FERMT1 gene variants to improve genotype-phenotype correlations.

This study defines spatial and molecular correlates of TIL manufacturing success and establishes a genomics-enabled selection platform for adoptive T cell therapy. The profiling approach is now being prospectively implemented in the GIANT clinical trial (NCT06816927), supporting its translational relevance and scalability across glioblastoma and other immune-excluded cancers.

This study defines spatial and molecular correlates of TIL manufacturing success and establishes a genomics-enabled selection platform for adoptive T cell therapy. The profiling approach is now being prospectively implemented in the GIANT clinical trial ( NCT06816927 ), supporting its translational relevance and scalability across glioblastoma and other immune-excluded cancers.

Combining targeted ECM softening with mechanotransduction inhibition strategy significantly attenuates tumor stemness and chemoresistance in vivo. Therefore, our findings highlight the role of ECM in regulating CSCs via biomechanical-dependent manner, suggesting the ECM/ITGB1/FERMT1/Wnt axis as a promising therapeutic target for CSCs therapy.

Additionally, administering SGC2085, a CARM1 inhibitor, effectively suppressed the malignant behaviors of HCC cells. To summarize, our findings provided strong evidence that CARM1 can serve as a key oncoprotein; thus, it holds promise as a therapeutic target for HCC.