Abstract
Actin-like protein 8 (ACTL8) is a member of the cancer-testis antigens (CTA) family, which is mainly localized in the cytoplasm and generally expressed in the testis. The association between ACTL8 and various types of cancer, including glioblastoma and breast cancer, has previously been demonstrated. However, whether ACTL8 is involved in the development of head and neck squamous cell carcinoma (HNSCC) remains unknown. In the present study, the expression of ACTL8 in patients with HNSCC was analyzed in The Cancer Genome Atlas (TCGA) dataset, clinical tissues and cell lines. Correlations between the expression levels of ACTL8 and HNSCC clinical outcomes were analyzed with the Kaplan-Meier method and the Cox proportional hazards model. Cell Counting Kit-8, plate colony formation and Transwell assays were used to assess the effects of ACTL8 interference on the proliferation, migration and invasion of HNSCC PCI-13 cells. Reverse transcription-quantitative polymerase chain reaction and western blotting were used to evaluate the expression levels of ACTL8 in PCI-13 cells. Furthermore, alterations in the expression levels of key proteins in the phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/RAC-α protein kinase B (AKT) signaling pathway were determined by western blotting. Increased expression of ACTL8 in HNSCC was observed in TCGA dataset, cancerous tissue samples and HNSCC cell line. Cox regression analysis indicated that ACTL8 expression could be regarded as an independent prognostic factor for HNSCC, since increased expression of ACTL8 was associated with a poor prognosis. Knocking down ACTL8 markedly inhibited the proliferation, invasion and migration of PCI-13 cells. Additionally, activation of the PI3K/AKT signaling pathway was suppressed by reduced expression levels of certain key proteins in this pathway. The present data indicate that ACTL8 serves a role in the progression and clinical prognosis of HNSCC. Therefore, ACTL8 may be a potential prognostic marker and novel therapeutic target for HNSCC.
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