Knockdown of tumor protein D52-like 2 induces cell growth inhibition and apoptosis in oral squamous cell carcinoma.

Abstract

Tumor protein D52-like 2 (TPD52L2) and its family members form homo- and hetero-meric complexes essential for cell proliferation in multiple human cancers. TPD52L2 is involved in cell migration and attachment in oral squamous cell carcinoma (OSCC). To confirm the role of TPD52L2 in OSCC, we employed the lentivirus-delivered small interfering RNA (siRNA) technique to knock down TPD52L2 expression in two OSCC cell lines, CAL27, and KB. Knockdown of TPD52L2 by RNA interference markedly suppressed cell proliferation and colony formation. Cell cycle analysis showed that depletion of TPD52L2 led to CAL27 cells arrest in the S phase. We found an excessive accumulation of cells in the sub-G1 phase, which can represent apoptotic cells. TPD52L2 silencing also induced the cleavage of PARP. These results suggest that TPD52L2 is involved in OSCC cell growth and serves as a potential therapeutic target in human OSCC.