Background Kinesin superfamily proteins (KIFs) serve as microtubule-dependent molecular motors, and are involved in the progression of many malignant tumors. In this study, we aimed to investigate the expression pattern and precise role of KIF21B in non-small cell lung cancer (NSCLC). Methods KIF21B expression in 72 cases of NSCLC tissues was measured by immunohistochemical staining (IHC). We used shRNA-KIF21B interference to silenced KIF21B in NSCLC cells. The biological roles of KIF21Bin the growth and metastasis abilities of NSCLC cells were measured by CCK8, colony formation and Hoechst/PI, wound-healing, and Transwell assays. The effect of KIF21B on tumor growth in vivo was examined using nude mice model. Results KIF21B was up-regulated in NSCLC tissues and correlated with pathological lymph node and pTNM stage, its high expression was predicted a poor prognosis of patients with NSCLC. Silencing of KIF21B mediated by lentivirus-delivered shRNA significantly inhibited the proliferation ability of H1299 cells. Moreover, KIF21B knockdown increased H1299 cell apoptosis through modulating the Bcl-2/Bax and active Caspase 3 expression. KIF21B knockdown decreased p-Akt expression and Cyclin D1 expression in H1299 cells. In addition, silencing of KIF21B impeded H1299 cell migration and invasion. Further, silencing of KIF 21B dramatically inhibited xenograft growth in BALB/c nude mice. Conclusions These results reveal that KIF21B is up-regulated in NSCLC and acts as an oncogene in the NSCLC progression.
Epidermolysis bullosa acquisita (EBA) is a rare, acquired, subepidermal blistering disease characterized by autoantibodies directed against type VII collagen, the major component of anchoring fibrils. We report a 5-year-old Chinese boy who presented with extensive lesions consisting of disseminated pruritic vesicles and tense blisters. The diagnosis of EBA was confirmed by histopathology, immunofluorescence, and immunoblotting analysis. The disease was controlled with a combination of prednisone and dapsone.
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