CAPG (Capping Actin Protein, Gelsolin Like)

Clinical specimens have confirmed that NCAPG2 is highly expressed in EOC tissues and is closely related to the clinical stage. High expression of NCAPG2 can promote the progression of EOC and may serve as a potential novel therapeutic target for EOC.

Thus, USP52 hampered PCa cell development and stemness through removing ubiquitination of RBM5 to control the expression of NCAPG2. USP52 may be used as a therapeutic target for PCa.

We developed a reusable multimodal diagnostic framework with candidate biomarkers and a radiomics tool to facilitate the early detection and risk stratification of HCC.

Bladder cancer patients face an elevated CVD death risk due to high CAPG protein expression, which can raise serum CAPG levels and harm cardiomyocytes.

Moreover, NCAPG promoted GPX4 expression in a NSUN2-dependent manner, which also promoted resistance to ferroptosis in HCC. Collectively, the current study identified NCAPG protected HCC cells from undergoing ferroptosis, emphasizing NCAPG as an optional target for potentially developing anti-cancer therapy and improving the effects of ferroptosis in HCC treatment.

PBK is a key regulator of pancreatic cancer and interacts with NCAPG2 to promote tumor progression, suggesting its value as a potential biomarker and therapeutic target for pancreatic cancer.

In vivo, CAPG knockdown in combination with Dox treatment significantly inhibited tumour growth in nude mouse models (***p < 0.01). These findings suggest that CAPG is a pivotal regulator of HCC progression and chemoresistance, offering a promising prognostic biomarker and combinatorial therapeutic target to overcome Dox resistance in clinical settings.

Mechanistically, CAPG promoted gene expression by inducing WDR74 transcription, which modulated the interaction between p53 and MDM2, resulting in p53 degradation. Our findings demonstrate that CAPG drives tumor proliferation and sorafenib resistance by inhibiting ferroptosis, suggesting that CAPG may serve as a promising target in HCC.

Our findings suggest that NCAPG, UBE2C, CDC20, CDK1, and SPP1 may serve as prognostic biomarkers for AML management, especially through their interaction with the p53 pathway in disease progression. These insights underscore the potential for targeting the p53 pathway and integrating these biomarkers to enhance outcomes for AML patients.

In conclusion, we have identified that CAFs-derived lactate promoted GC progression and clarified its mechanism, proposing the H3K18la-ASPM-NCAPG axis. Daturilin could enhance the therapeutic efficacy of anti-PD-1 treatment. This offers innovative perspectives on the complex role of CAFs in the TME and the influence of lactate on tumor progression.

High expression of RPL35A is linked to poor prognosis in hepatocellular carcinoma. The regulation of NCAPG2 by RPL35A may represent a critical mechanism underlying RPL35A-driven tumor progression. Targeting the RPL35A/NCAPG2 pathway may offer a promising therapeutic strategy for HCC treatment.

Furthermore, we discovered that the disordered domain of NCAPG (D-NCAPG) serves as the specific binding sites for SIP binding. In conclusion, this study reveals the underlying mechanism by which NCAPG promotes EMT in HCC, which may be useful in the treatment of NCAPG-expressing HCC.