Background
Collagen type VI alpha 6 chain (COL6A6) plays a vital role in maintaining cell structural integrity and regulating cell function. It has been proven to be a tumor suppressor gene and molecular therapeutic target. However, the mechanism of COL6A6 in non-small cell lung cancer (NSCLC) has not been elucidated. The
Conclusions
Our study illustrates that COL6A6 is a tumor suppressor gene in NSCLC and is involved in NSCLC tumorigenesis by regulating the JAK signalling pathway. Therefore, COL6A6 holds promise as a molecular therapeutic target for NSCLC.
Methods
We analyzed the expression of COL6A6 in NSCLC using public databases and verified the findings in NSCLC tissues and cells. The protein expression of COL6A6 was evaluated by Western blot. The CCK8 and Transwell assays were used to assess the invasion ability of NSCLC cells after COL6A6 knockdown. At the same time, we discussed the role of the JAK signalling pathway that may be related to COL6A6.
Results
Bioinformatics analysis showed that COL6A6 expression was downregulated in NSCLC, and its high expression was associated with a better prognosis of NSCLC. In vitro, the expression of COL6A6 in NSCLC tissues was significantly lower than that in adjacent tissues. Furthermore, COL6A6 knockout accelerated the proliferation, invasion, and migration of NSCLC cells and activated the JAK signalling pathway. Conclusions: Our study illustrates that COL6A6 is a tumor suppressor gene in NSCLC and is involved in NSCLC tumorigenesis by regulating the JAK signalling pathway. Therefore, COL6A6 holds promise as a molecular therapeutic target for NSCLC.