DIAPH1 Is Upregulated and Inhibits Cell Apoptosis through ATRp53Caspase-3 Signaling Pathway in Laryngeal Squamous Cell Carcinoma

Abstract EN

Cancer bioinformatics has been used to screen possible key cancer genes and pathways.

Here, through bioinformatics analysis, we found that high expression of diaphanous related formin 1 (DIAPH1) was associated with poor overall survival in head and neck squamous cell carcinoma and laryngeal squamous cell carcinoma (LSCC).

The effect of DIAPH1 in LSCC has not been previously investigated.

Therefore, we evaluated the expression, function, and molecular mechanisms of DIAPH1 in LSCC.

Immunohistochemistry and western blot analysis confirmed the significant upregulation of DIAPH1 in LSCC.

We used DIAPH1 RNA interference to construct two DIAPH1-knockdown LSCC cell lines, AMC-HN-8 and FD-LSC-1, and validated the knockdown efficiency.

Flow cytometry data showed that DIAPH1 inhibited apoptosis.

Further, western blot analysis revealed that DIAPH1 knockdown increased the protein levels of ATR, p-p53, Bax, and cleaved caspase-3, -8, and -9.

Thus, DIAPH1 is upregulated in LSCC and may act as an oncogene by inhibiting apoptosis through the ATR/p53/caspase-3 pathway in LSCC cells.