ARPC1B (Actin Related Protein 2/3 Complex Subunit 1B)

Crucially, the re-expression of ARPC1B in NAA30-silenced cells effectively restored these malignant phenotypes. These findings highlight the critical role of the NR2C2-NAA30-ARPC1B axis in ovarian cancer progression and provide more foundation for the development of more effective treatment strategies for patients with ovarian cancer.

ARPC1B emerges as an essential oncogenic factor in ccRCC by stimulating EMT and activating the Wnt/β-catenin pathway, ultimately enhancing tumor aggressiveness and metastatic potential. Thus, targeting ARPC1B represents a promising therapeutic strategy, warranting further exploration in ccRCC management.

In vitro cytotoxicity, ex vivo organoid cultures, in vivo xenograft and orthotopic gemcitabine-resistant pancreatic cancer model demonstrated that combination therapy of gemcitabine plus CK-636 showed a superior anti-tumor effect compared with gemcitabine monotherapy. Our study demonstrated that CK-636 can act as a rational adjuvant to overcome gemcitabine resistance in pancreatic cancer therapy.

Validations included RT-qPCR, ChIP-qPCR, immunofluorescence, dual-luciferase assays, and immunohistochemistry. The YY1/BLACAT1/miR-605-3p axis drives GBM progression, offering therapeutic potential.

Inhibiting ARPC1B reshaped the immunosuppressive microenvironment and increased the efficacy of ICB in glioblastoma models. This study highlights the important role of ARPC1B in macrophage-mediated immunosuppression and proposes a combination treatment regimen for glioblastoma immunotherapy.

ARPC1B overexpression is associated with poor prognosis, altered immune status, and drug sensitivity in ccRCC. Furthermore, ARPC1B promotes the malignant behavior of ccRCC cells and holds potential as a prognostic biomarker and therapeutic target for ccRCC.

The prognostic model comprising ARPC1B, BATF, CCL2, and COTL1 can effectively identify high-risk EC patients and predict their response to immunotherapy, demonstrating significant clinical potential. These genes are implicated in EC development and immune infiltration, with BATF emerging as a potential therapeutic target for EC.

Mechanistically, circZMYM2 competitively bound to FXR1 to regulate the translation of NACA and ARPC1B. CircZMYM2 may be a crucial regulator of OS tumorigenesis and a potential diagnostic and therapeutic biomarker for OS patients.

Further experiments showed that ARPC1B can affect the proliferation, apoptosis, migration, and invasion of OV cells through the AKT/PI3K/mTOR pathway. ARPC1B is a biomarker for immune suppression, prognosis, clinical staging, and drug resistance, providing new insights for cancer therapeutics.

In many malignancies, particularly READ, ARPC1B overexpression is associated with immune cell infiltration and a poor prognosis. These results imply that the molecular biomarker ARPC1B may be used to assess the prognosis and immune infiltration of patients with READ.

ARPC1B expression levels showed associations with immune cell populations within the GBM microenvironment. ARPC1B can regulating immune infiltration in the GBM microenvironment, indicating its potential as a novel therapeutic target for GBM.