NAP1L1 (Nucleosome Assembly Protein 1 Like 1)

This neoplasm showed typical morphology with nests of tumor cells with cribriform and papillary architecture and a classic immunohistochemical profile with tumor cells positive for S100 and p63 while negative for p40. Molecular studies showed a NAP1L1::PRKD1 fusion, which has not been previously detected in cribriform adenocarcinoma.

ICDRS predicted differential therapeutic vulnerabilities: low-risk patients showed enhanced sensitivity to standard immunotherapy-compatible treatments including sorafenib and doxorubicin, while high-risk patients demonstrated preferential sensitivity to EGFR-targeted therapies. This model provides robust stratification for immunotherapy selection and advances precision medicine in HCC management. Future clinical translation includes prospective validation and development of companion diagnostics, offering potential pathways for personalized HCC treatment implementation.

Our findings demonstrate that FBXW7-mediated NAP1L1 degradation suppresses HDGF-p62 signaling, thereby inducing autophagy and enhancing DDP chemosensitivity. These results underscore the potential of NAP1L1 and FBXW7 as therapeutic targets for NPC treatment.

To sum up, our study demonstrated that NAP1L1 promoted the malignant phenotypes of EC cells via recruiting EP300 to promote DDX5 acetylation, thus activating the Wnt/β-catenin signaling pathway. Implications: Our research findings indicate that targeting the NAP1L1/EP300/DX5 axis might be a new potential treatment option for endometrial cancer.

CircDCAF8 facilitates HCC proliferation and metastasis via the miR-217/NAP1L1 axis. Meanwhile, circDCAF8 can promote angiogenesis and drive resistance to regorafenib, making it a viable therapeutic target for HCC patients.

In conclusion, this study reveals a novel mechanism through which NAP1L1 regulates the ubiquitination of BIRC2 through UBR4, thereby determining the progression of HCC. Based on this mechanism, suppression of NAP1L1 may inhibit tumour progression in patients with HCC with high protein expression of NAP1L1 or BIRC2.

Regardless of the fusion partner, patients with AML harboring MLLT10 fusions exhibit very high-risk features and should be prioritized for alternative therapeutic interventions. Clinical trials #NCT00372593 NCT01371981.

Our findings revealed for the first time that serum levels for NAP1L1 was overexpressed in the gastric cancer, as also correlated with the disease progression. NAP1L1 seems to be a potential biomarker for gastric cancer, providing clinically important information on early diagnosis and risk stratification.

High plasma levels of a 9-gene signature (BECN1, PRKCB, COPA, TSC22D3, MAP2K3, UQCRHL, PTMAP4, EHD1, NAP1L1 pseudogene) and a 5-gene signature (FTH1P7, PTMAP4, ATF4, FTH1P8, ARMC7) were significantly associated with inferior progression-free and overall survival in DLBCL patients, respectively, independent of the NCCN-IPI score. Total RNA sequencing of blood plasma samples allows the analysis of the cell-free transcriptome in DLBCL and PMBCL patients and demonstrates its unexplored potential in identifying diagnostic, cell-of-origin, and prognostic cfRNA biomarkers.

The present research aimed to investigate the role of MYH9 in glioma and determine whether MYH9 is involved in the temozolomide chemoresistance of glioma cells...Altogether, our results show that MYH9 plays a role in glioma progression by regulating NAP1L1 deubiquitination. Thus, targeting MYH9 is a potential therapeutic strategy for the clinical treatment of glioma in the future.

Moreover, Nucleosome Assembly Protein 1 Like 1 (NAP1L1) is a downstream target for miR-770-5p and essential for circPUM1-mediated cisplatin resistance and NK cell cytotoxicity in OSCC cells. The network composed of SP2, circPUM1, miR-770-5p and NAP1L1 in OSCC appears to be a promising avenue for the development of novel targets for diagnosing or treating OSCC.

Finally, transfection with HDGF or DDX5 restores cell growth in NAP1L1-knockdown colon cancer cells by upregulating DDX5/β-catenin/CCND1 signaling. Our study demonstrates that NAP1L1 functions as a potential oncogene that promotes colon cancer tumorigenesis by binding to HDGF, which stimulates DDX5/β-catenin/CCND1 signaling.