ACTN4 (Actinin Alpha 4)

This study suggests that actinin-4 plays a role in the progression of endometrial carcinoma, particularly influencing tumor aggressiveness and progression-free survival.

Overall survival and progression-free survival were numerically shorter for patients with ACTN4 positivity than for those with ACTN4 negativity in fluorescence in situ hybridization. The findings suggest that ACTN4 amplification and actinin-4 protein expression are prognostic markers for poor osimertinib efficacy in epidermal growth factor receptor-mutant non-small cell lung cancer.

Not applicable. The online version contains supplementary material available at 10.1186/s12882-025-04433-4.

Two cisplatin-resistant osteosarcoma cell line models (U2OS-DDPr and 143B-DDPr) were established by culturing parental U2OS and 143B cells with escalating cisplatin concentrations (250 ng/mL to 2.5 µg/mL) over a 6-month period...Furthermore, we found that wortmannin, an inhibitor of ACTN4, could markedly block the effect of SOCS1 silencing on osteosarcoma aggressiveness. In conclusion, SOCS1 deletion promotes stemness and chemoresistance in osteosarcoma by inhibiting ACTN4 ubiquitination and degradation, which offers promising therapeutic targets for potentiating chemosensitivity in osteosarcoma.

Taken together, our findings reveal for the first time a new mechanism by which circACTN4 could promote oncogenesis and the development of BC by increasing the AcH4 of MYC target genes via TIP60. Therefore, circACTN4 could be a novel target for BC diagnosis and remedy.

CAFs-derived COL17A1 promoted GEM resistance and tumorigenesis in PC by interacting with ACTN4, suggesting a new method for overcoming GEM resistance in PC.

Mechanistically, circACTN4 served as a rival internal RNA for miR-424 5p, controlling NCAPG level and initiating the Wnt/β-catenin signaling routes, which in turn impacted the EMT machinery in HCC. According to our surveys, the circACTN4/miR-424 5p/NCAPG axis could be an intriguing candidate for therapy to address the treatment of HCC.

Experimental procedures demonstrated that silencing SDCBP attenuated cell growth, glucose metabolism and extracellular acidification rate, accompanied by decreased expression of p-AKT, p-ERK1/2, LDHA and Vimentin. The established 8-gene signature holds promise as a tool for predicting NMIBC recurrence, while targeting SDCBP may represent a potential strategy for delaying disease relapse.

Cyclophosphamide and ethinyl estradiol may be potential drugs affected by DEDRGs for future research. This study found that ACTB, ACTN4, INF2, and MYL6 are closely related to PD and pan-cancer and can be used as candidate genes for the diagnosis, prognosis, and therapeutic biomarkers of neurodegenerative diseases and cancers.

ACTN4 knockdown suppressed the formation of ruffle-edge lamellipodia and cell migration during wound healing in A549 monolayer cultures. Additionally, membrane-type 1 matrix metalloproteinase was observed in the membrane ruffles, suggesting that ruffle-edge lamellipodia have the ability to degrade the extracellular matrix and may contribute to active cell migration/invasion in certain cancer cell types.

A WB and immunohistochemistry staining comparison of primary and disseminated lesions of TETs using surgical specimens showed upregulated expression of ACTN4, β-catenin, and Slug proteins in disseminated lesions. In summary, our study suggests ACTN4 is associated with malignant potential characteristics such as invasion and dissemination in TETs via the β-catenin/Slug pathway.

Similar behavior was observed in knockdown cells expressing K255E ACTN4, which is primarily localized to the cytosol. Together, our findings establish a role for nuclear ACTN4 in regulating invasiveness via modulation of EMT.