ACTR2 (Actin Related Protein 2)

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.

Our study objectively demonstrated the pharmacological effects of CLS in promoting the wound healing of anal fistula and investigated its mechanisms in terms of regulating the immune inflammatory process of macrophages increases signal communication with fibroblasts while promoting fibroblast transformation.

Our results reveal the F-actin assembly is inhibited by silibinin, and this results in G2/M cell cycle arrest in human breast cancer cells, providing new ideas for anti-cancer therapies including TNBCs. Abbreviations: ABPs, actin binding proteins; ARP2, actin-related protein2; Capza1, capping actin protein of muscle Z-line subunit alpha 1; CDC2, Cell Division Cycle protein 2/CDK1, Cyclin-Dependent Kinase 1; CDKi, cyclin-dependent kinase inhibitors; CDKs, cyclin-dependent kinases; CETSA, cellular thermal shift assay; CFL1, cofilin 1; Cyto D, Cytochalasin D; DARTS, drug affinity responsive target stability; DIAPH3, diaphanous related formin 3; DMEM, Dulbecco's Modified Eagle medium; ER, estrogen receptor; F-actin, filamentous actin; FBS, fetal bovine serum; G-actin, globular actin; GSN, gelsolin; HER2, human epidermal growth factor receptor 2; LAMP1, lysosomal associated membrane protein 1; NLS, nuclear localization signal; PDB, protein data bank; PFN1, profilin 1; PR, progesterone receptor; qRT-PCR, quantitative real-time polymerase chain reaction; RT, room temperature; Sili, silibinin; si-RNAs, small interfering RNAs; TNBC, triple-negative breast cancer; VP, verteporfin; YAP, Yes-associated protein.

This study demonstrates the utility of applying a linkage analysis framework to familial WES data for identifying genomic regions and candidate genes that may contribute to MM/MGUS predisposition. These findings provide new insight into the inherited risk and etiology of familial MM and MGUS.

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.

LDHA is identified as a critical key gene with a significant impact on immunotherapy outcomes, presenting a potential therapeutic target. These insights offer new biomarkers and targeted strategies for personalized immune therapy.

Lowering CRLF3 inhibited HCC xenografted tumor growth in nude mice. Through its targeted binding to ACTR2, CRLF3 aids in the growth and immune escape of HCC cells.

Tumor cells have a range of monoallelic and biallelic expression patterns in both imprinted and non-imprinted genes and are likely affected by the complex interplay among changes in allelic expression, sequence variants, copy number changes, and expression changes of biologically important genes. Multiple isoform-specific patterns of allelic expression were associated with drug response, indicating complex mechanisms of cancer chemoresistance.

LQZ is effective in treating AD by alleviating skin barrier damage and inflammatory reactions. Its anti-AD properties of LQZ may be attributed to the inhibition of the FcγR-mediated phagocytic pathway.

Aurora-A overexpression upregulates the expression of ARPC4 by activating the NF-κBp65 signaling pathway, thereby promoting migration, invasion and EMT of HeLa cells.

By light microscopy, the tumor showed cribriform and tubular patterns with obvious perineural and intraneural invasion. The findings remind us that salivary gland tumors without MYB/MYBL1 fusion genes could still be ACC if they have a rearrangement involving genes adjacent to MYB/MYBL1 genes.

Furthermore, the Rac1 inhibitor did not block increased cell migration in PC3 cells overexpressing constitutively active Gαi2. We conclude that activated Gαi2 plays a crucial role in cell migration in prostate cancer cells independent of Rac1 activation.