RNAi Targeting-STIL Suppresses Cell Growth and Induces Apoptosis of Lung Cancer NCI-H1299 Cells via Inactivation of Akt/SAPK/TAK1 Pathways

Abstract Background: Gradually emerged studies demonstrated that SCL/TAL1 interrupting locus (STIL or SIL) is upregulated in multiple kinds of fatal tumors; at present, there is no clean understanding about the role of STIL in lung adenocarcinoma cells. This study aimed to discover the significance of STIL in lung adenocarcinoma, so as to find a potential gene target for diagnosis and therapy. Methods: STIL expression in lung adenocarcinoma tissue and clinical pathological characteristic was analyzed using the online databases, UALCAN and GEPIA. Lentivirus STIL-shRNA was manufactured and transducted into lung adenocarcinoma cells to seek and analyze the effects on tumor phenotype. The cell proliferation was assessed using Cellomics Array Scan imaging assay, and colony-formation assay, respectively. The apoptosis was detected by flow cytometry assay. Moreover, the antibody array of PathScan Cancer Phenotype, PathScan stress and apoptosis pathway was used to explore relevant molecular mechanisms following STIL knockdown in NCI-H1299 cells. Results: The clinical pathological characteristic assay showed that STIL is upregulated in lung adenocarcinoma tissues, and this trend was associated with cancer stage1 and histological subtypes. Silencing experiment showed that downregulation of STIL could inhibit cell growth and colony formation, induce cell apoptosis, and a G2 phase arrest effect significantly, and antibody array detection revealed that p-Bad were upregulated, and p-Akt, p-Bad, p-HSP27, p-SAPK/JNK, p-TAK1, Vimentin, CD45, PCNA and Ki-67 were downregulated significantly after STIL silenced in NCI-H1299 cells.Conclusions: In conclusion, STIL is overexpressed in lung adenocarcinoma tissues compared with normal lung tissue. Knockdown of STIL could inhibit cell growth and colony formation ability, promote apoptosis via Akt/SAPK/TAK1 signal pathways inactivation.