Establishment and Preliminary Analysis of Cell Line A549 with Stable Knockdown of TNIK Expression
SUN Xuehua1,2, YIN Xun1,2, WANG Ru1,2, ZHANG Tao1,2, CHEN Quan3, ZHANG Chundong1,2*
TNIK (TRAF2 and NCK interacting kinase), a member of the family of serine/threonine kinase, has played a key role in many physiological and pathological process. Recent studies have found that TNIK is highly expressed in lung squamous cell carcinoma tissues and drives cancer cell proliferation and other malignant phenotypes, but its role in lung adenocarcinoma is still poorly understood. In this study, a lung adenocarcinoma A549 cell line with stable knockdown TNIK expression were constructed. Flow cytometry showed that the cell cycle was arrested and apoptosis was induced. Cell proliferation and movement experiments proved that the proliferation and migration of lung cancer cells were significantly inhibited. Further immunofluorescence staining analysis showed that stable knockdown of TNIK expression could induce disorder of cell actin cytoskeleton and inhibit dynamic turnover (assembly/depolymerization) of focal adhesions. In conclusion, TNIK in lung adenocarcinoma cells may influence the dynamic turnover of focal adhesions and ultimately control cell proliferation and migration by regulating the arrangement of actin cytoskeleton. It is speculated that the highly expressed TNIK in lung adenocarcinoma cells can maintain the malignant phenotype of cancer cells by regulating the actin cytoskeleton system.
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