COL11A1 Was Involved in Cell Proliferation, Apoptosis and Migration in Non-Small Cell Lung Cancer Cells

Type XI collagen (COL11A1) was reported to associate with malignancy in several cancer types, whereas its role in lung cancer is not fully understood. Therefore, the present study aimed to explore the expression level and biological role of COL11A1 in lung cancer cells.

Gene Expression Omnibus (GEO) database containing 6 lung cancer tissues and normal lung tissues was used to identify potential aberrantly expressed genes. The expression of COL11A1, apoptosis related genes, cell cycle related genes and migration associated genes at the protein level were evaluated by western blot and at the mRNA level was determined by real-time PCR in lung cancer cell lines. Furthermore, the expression of COL11A1 was silenced by siRNA, and cell viability was detected by Cell counting kit-8 (CCK-8) assay. Moreover, cell apoptosis and cell cycle were determined by flow cytometry. In addition, transwell and wound-healing assay were applied to determine cell migration ability.

GEO analysis suggests that COL11A1 was highly expressed in patients with lung cancer, which was consistent with the results in lung cancer cell lines. COL11A1 knockdown in lung cancer cells significantly lowered the colony formation ability, augmented cell apoptosis rate and elevated the expression of cleaved caspase-3, cleaved caspase-9, Bax, P21 and the expression of Bcl-2, CyclinD1, CDK2 and CDK-4 was significantly downregulated (all p < 0.05). Moreover, post-COL11A1 knockdown, the cell wound-healing and migration ability was significantly impaired, which also supported by the upregulation of E-Cadherin and downregulation of N-Cadherin, Vimentin and Snail (all p < 0.05). Furthermore, we also found that COL11A1 knockdown decreased the expression of p-AKT, p-PI3K and p-ERK.

The present study revealed that COL11A1 may contribute to the malignancy and involve in the pathogenesis of lung cancer.