| 摘要: | Lung cancer is the most frequently incident and malignant cancer in both men and women, causing life-threatening to patients who suffer from this disease. Among all types of lung cancer, non-small cell lung cancer (NSCLC) is the most frequent subtype, with aggressive characteristics and poor treatment response. Previous studies revealed the upregulation of ZBED3 in lung cancer, and its expression also correlates with poor prognosis, however, this finding conflicts with the clinical data from the cancer genome atlas (TCGA) database. Furthermore, the mechanism ZBED3 driving lung adenocarcinoma, as well as its downstream activated pathway, still remains unclear. To get insight into the mechanism in which ZBED3 involves in lung cancer, we first examine the function of ZBED3 in non-small cell lung cancer progression. The ZBED3 was overexpressed using virus transduction, while CRISPR/Cas9 was employed to knockout ZBED3 in lung cancer cell lines. The functional assays, including MTT, colonization, and invasion assays, demonstrated that ZBED3 is involved in cancer proliferation, and invasion. To be specific, ZBED3 knockout dramatically exhibited the colony formation and invasion ability of NCI-H661 and A549 cells, while ZBED3 overexpression significantly increased these abilities in A549 cell lines.
In addition, non-small cell lung cancer (NSCLC) is fast-growing and highly invasive; western blot results indicated that ZBED3 knockout attenuated cancer cell proliferation suppressing AKT phosphorylation. Besides, ZBED3 knockout inhibited the metastasis progression of NSCLC cells through EMT markers by upregulating epithelial marker and downregulating mesenchymal markers. These evidences suggest that ZBED3 plays an essential role in the proliferation, invasion, and metastasis of NSCLC cancer. In sum, we expect to figure out a prognostic target for lung cancer therapeutics. |
