BackgroundKinesin family member 26B (KIF26B) plays a key role in the development and progression of many human cancers. However, the role and underlying mechanisms of KIF26B in breast cancer cells remain unknown.Materials and methodsIn this study, we inhibited the expression of KIF26B in MDA-MB-231 and MCF-7 cells using lentivirus-delivered shRNA.ResultsLentivirus-mediated KIF26B knockdown significantly suppressed cell proliferation, colony formation, migration, and invasion. Furthermore, cell cycle analyses revealed that the percentage of cells in the G0/G1 phase was significantly increased in KIF26B knockdown cells. Moreover, the knockdown of KIF26B significantly promoted cell apoptosis via the upregulation of cleaved caspase-3 and Bax.ConclusionOur data indicate that KIF26B plays a pivotal role in tumor growth and metastasis in breast cancer cells and may be a potential therapeutic target for treating breast cancer.
V-myc avian myelocytomatosis viral oncogene neuroblastoma derived homolog (MYCN) is an oncogene that is known amplified and overexpressed in different human malignancies including small cell lung cancer. However, the role of MYCN in non-small cell lung cancer (NSCLC) development remains elusive. In the present study, Western blot and immunohistochemistry assays demonstrated that MYCN was overexpressed in NSCLC tumor tissues and cell lines. In addition, immunohistochemistry analysis revealed that upregulation of MYCN expression was positively correlated with a more invasive tumor phenotype and poor prognosis. In vitro studies using serum starvation-refeeding experiment and MYCN-siRNA transfection assay demonstrated that MYCN expression promoted proliferation of NSCLC cells, while MYCN knockdown led to decreased cell growth resulted from growth arrest of cell cycle at G0/G1 phase. Furthermore, upregulation and knockdown of sex-determining region Y-box 2 (SRY) (SOX2), which was a well-known oncogene, confirmed that MYCN might be a downstream gene of the transcription factor SOX2. Collectively, our finding suggested that MYCN might contribute to the progression of NSCLC by enhancing cell proliferation, and that targeting MYCN might provide beneficial effects for the clinical therapy of NSCLC.
HES5 is a transcription factor activated downstream of the Notch pathway and regulates cell differentiation in multiple tissues. Disruption of its normal expression has been associated with developmental diseases and cancer. But its role in non-small cell lung cancer (NSCLC) remains elusive. Western blot analysis and immunohistochemistry assays demonstrated that HES5 expression was frequently increased in NSCLC tumor tissues and cell lines. Moreover, immunohistochemistry analysis revealed that upregulation of HES5 expression was positively correlated with a more invasive tumor phenotype and poor prognosis. Immunoprecipitation assay indicated that HES5 directly interacted with STAT3. In addition, depletion of HES5 resulted in inhibited phosphorylation of STAT3 and decreased expression of the downstream genes. In vitro studies, using serum starvation-refeeding experiment and HES5-siRNA transfection assay demonstrated that HES5 expression promoted proliferation of NSCLC cells, while HES5 knockdown caused growth arrest of cell cycle at G0/G1 phase, decreased rate of colony formation and alleviated cellular apoptosis. Taken together, out data have delineated that HES5 might contribute to the proliferation of NSCLC by STAT3 signaling.
Neuropsychiatric disorder-associated disrupted-in-schizophrenia-1 (DISC1) activates Wnt/β-catenin signaling by inhibiting glycogen synthase kinase 3 beta (GSK3β) phosphorylation, and may promote neural progenitor cell and pancreatic β-cell proliferation. The present study found that DISC1 promotes non-small cell lung cancer (NSCLC) cell growth. Western blotting and immunohistochemistry analyses showed that DISC1 was highly expressed in NSCLC cell lines and patient tissues. DISC1 expression was negatively associated with phosphorylated (p-) GSK3β, but positively correlated with a more invasive tumor phenotype and predicted poor NSCLC patient prognosis. siRNA-mediated DISC1 silencing increased p-GSK3β expression and decreased expression of β-catenin and Cyclin D1, while DISC1 upregulation produced the opposite results. DISC1 knockdown also reduced NSCLC cell proliferation rates in vitro. These results suggest that DISC1 promotes NSCLC growth, likely through GSK3β/β-catenin signaling, and that DISC1 may function as an oncogene and novel anti-NSCLC therapeutic target.
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