Abstract
The involvement of long noncoding RNA (lncRNA) SNHG16 has been reported in several human cancers. Notwithstanding, the role of lncRNA SNHG16 is yet largely unknown in human lung cancer. Consequently, this study was undertaken to investigate the role and therapeutic potential of SNHG16 in human lung cancer. The results showed a significant (P < 0.05) transcriptional upregulation of SNHG16 in lung cancer tissues and cell lines. However, downregulation of SNHG16 resulted in significant (P < 0.05) inhibition of lung cancer A549 and SK-LU-1 cell proliferation. DAPI and annexin V/PI assays revealed apoptosis to be responsible for inhibition of cell proliferation and colony formation observed upon SNHG16 knockdown. This was accompanied by enhancement of Bax and suppression of Bcl-2 expression in A549 and SK-LU-1 cells. Transwell assays revealed that silencing of SNHG16 also significantly (P < 0.05) inhibited migration and invasion of A549 and SK-LU-1 cells. Bioinformatic analysis revealed that SNHG16 interacted with ALDH2 to exert its effects in human lung cancer cells. The expression of ALDH2 was found to be significantly (P < 0.05) suppressed in human lung cancer tissues and cell lines. Overexpression of ALDH2 inhibited the proliferation and colony formation of the A549 and SK-LU-1 cells. However, silencing of ALDH2 could avoid the tumor-suppressive effects of SNHG16 knockdown. Finally, SNHG16 silencing was also found to inhibit in vivo tumor growth. Collectively, the study unveils the molecular role of SNHG16 in regulating the development of lung cancer by interacting with ALDH2.