FIGNL1 (Fidgetin Like 1)

Furthermore, we identify that the MMS22L-TONSL complex interacts with FIGNL1 and is critical for HR in BRCA2/FIGNL1 double-deficient cells. These findings identify a pathway for tightly regulating RAD51 activity to promote efficient HR, offering insights into mechanisms of chemoresistance in BRCA2-deficient tumors.

We observed significant differences in clinical characteristics, immune cell infiltration, gene mutation landscapes, immunotherapy responses, and drug sensitivity between the high-risk and low-risk groups. The novel E2Fs-based gene risk model shows significant potential for contributing to the evaluation of prognosis and predicting immunotherapeutic outcomes for colorectal cancer patients.

Their involvement in these processes underscores their role as potential biomarkers for certain cancers as well as therapeutic targets for diseases affecting the nervous system and cardiovascular development. All these evolutionary insights and functional distinctions of the FIGN family offer a comprehensive framework for understanding cytoskeletal regulation and its implications in health and disease.

Subsequent experiments demonstrated that FIGNL1-mediated P38 phosphorylation was contingent upon SPIDR interaction. These results implied that FIGNL1 was a potential anticancer drug target, which also offered a novel strategy for future CRC treatment.

RAD51 is the core component of HR, catalyzing the strand invasion and homology search. Here, we highlight recent findings on FIRRM and FIGNL1 as regulators of the dynamics of RAD51.

We identified eight hub genes (CCL2, CCR2, IL6, CSF3R, ATL2, SESN3, UROC1, FIGNL1), which may become early diagnostic and therapeutic targets for NAFLD and HCC. The pan-cancer analysis of UROC1 provides new evidence for its broad application prospects in the field of HCC and other cancers.

Our study revealed that FIGNL1 could modulate the ECM-receptor interaction pathway through the regulation of HMMR, thus regulating the formation of HCC.

In the two decades since their first report, there has been great progress in our understanding of the fidgetins; however, there is still much left unknown about this unusual family. This review aims to consolidate the present body of knowledge of the fidgetin family of MSEs and to inspire deeper exploration into the fidgetins and the MSEs as a whole.

Together, our data demonstrate that ZmBRCA2 and ZmFIGL1 act coordinately to regulate the dynamics of RAD51/DMC1-dependent DSB repair to promote crossover formation in maize. This conclusion is surprisingly different from the antagonistic roles of BRCA2 and FIGL1 in Arabidopsis, implying that although key factors that control crossover formation are evolutionarily conserved, specific characteristics have been adopted in diverse plant species.

FIGNL1 is associated with poor prognosis in NSCLC, and cisplatin resistance may be involved. These observations provide a clinical basis for exploring FIGNL1 as a potential biomarker for cisplatin resistance in NSCLC.