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Open access Oct 2026

CPNE8 Suppresses Hepatocellular Carcinoma Progression Through Downregulation of ITGB1/CDC42/PAK1 Signaling and an Altered Immune-Marker Profile

Background: Hepatocellular carcinoma (HCC) is among the most lethal malignancies, and its immunosuppressive microenvironment limits the efficacy of current therapies. The integrin β1 (ITGB1)-CDC42-p21-activated kinase 1 (PAK1) axis is an established driver of HCC progression; however, the role of copine 8 (CPNE8), a ca...

Xiao-Fang Zhao, Jing Meng, Li-Min Wang · 0 citations
Open access Oct 2026

ACOT7 promotes HNSCC progression by disrupting the AKT-MDM2-p53 axis

The functional role of ACOT7 was examined using an integrated approach, combining analysis of clinical datasets with in vitro and in vivo experiments, and MYC-associated regulation and changes in total AKT and p-MDM2 levels suggest a potential connection between ACOT7 and growth-related signaling.

Zhen-Ning Jin, Jia-Yi Peng, Diana Messadi et al. · 0 citations
Open access Sep 2026

XPR1 Promotes the Malignant Phenotypes of Thyroid Carcinoma Cells Partly Through NF-κB-Related Signaling

The results suggest that the pro-tumorigenic effects of XPR1 in thyroid carcinoma cells, manifested by increased cell growth, motility, invasiveness, and reduced susceptibility to apoptosis, may be partly associated with NF-κB signaling.

J. You, Tong-Xin Zou, Bo-Xiu Wang et al. · 0 citations
Sep 2026

METTL1/USP48 Axis Stabilizes LCN2 Expression to Promote the Malignant Phenotypes of Cutaneous Squamous Cell Carcinoma

Clinically, these findings identify the METTL1/USP48/LCN2 pathway as a potential therapeutic target for cSCC and elucidated a novel oncogenic axis in cSCC, wherein METTL1 stabilized USP48 mRNA through m7G methylation modification, and USP48 in turn deubiquitinated and stabilized LCN2 protein.

Xiu-Qi Li, Lin Shu, Xiao-Qiang Li et al. · 0 citations
Sep 2026

Targeting IGF2BP3-driven CSF1/CSF1R signaling disrupts the positive feedback loop between tumor cells and macrophages and inhibits HCC progression.

It is revealed that IGF2BP3 drives HCC malignancy by establishing a reciprocal interaction between tumor cells and macrophages via the CSF1/CSF1R signaling pathway, highlighting that therapeutic targeting of this axis may disrupt tumor-macrophage crosstalk and improve therapeutic efficacy.

Xiao-Ying Ji, Lin-Ran Zhang, Xiao-Xiao Zhu et al. · 0 citations

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