ARPC4 is a core subunit of the Arp2/3 complex, a multiprotein actin nucleator that mediates branched actin filament assembly in response to nucleation-promoting factors. In the cytoplasm, the Arp2/3 complex drives cell motility by organizing branched actin networks at the leading edge of lamellipodia. Beyond cytoplasmic functions, the complex promotes nuclear actin polymerization to regulate gene transcription and facilitate homologous recombination repair of DNA damage. Recent evidence indicates ARPC4 is critical for cancer cell invasion and metastasis across multiple malignancy types. In pancreatic ductal adenocarcinoma, the Arp2/3 complex mediates acinar-to-ductal metaplasia downstream of mTORC1 and mTORC2 signaling 1. ARPC4 overexpression correlates with lymph node metastasis in bladder cancer, and its knockdown attenuates cancer cell invasion and migration 2. In cervical cancer, Aurora-A promotes ARPC4 expression through NF-κB signaling to drive invasion and epithelial-mesenchymal transition 3. Conversely, ARPC4 loss-of-function causes a psoriasis-like epidermal disease marked by Nrf2 hyperactivation, suggesting the complex regulates keratinocyte differentiation 4. ARPC4 upregulation is also detected in oral squamous cell carcinoma and associates with poor prognosis 5. These findings position ARPC4 as a node integrating oncogenic signaling with actin-dependent cell migration, making it a candidate therapeutic target in metastatic cancers.