RESUMEN
Family with sequence similarity 129, member A (FAM129A), also called Niban or C1orf24, was initially identified from a rat model of hereditary renal carcinoma. FAM129A inhibited apoptosis and promoted migration and proliferation in human cancers. However, little is known about the downstream signaling during tumor progression. Our data showed that FAM129A played an oncogenic role in non-small cell lung carcinoma (NSCLC), which upregulated the protein levels of MMP2 and Cyclin D1 through activating the FAK signaling pathway. Treatment by FAK inhibitor counteracted the increase of MMP2 and Cyclin D1 expression following by FAM129A transfection through attenuating the phosphorylation of FAK. Results of immunohistochemistry revealed that the expression of FAM129A was significantly associated with larger tumor size (P=0.036), advanced TNM stage (P<0.001), and lymph node metastasis (P=0.001). Subsequent Kaplan-Meier analysis indicated that patients with FAM129A expression presented with poorer clinical outcome (P=0.001). Taken together, our results suggested that FAM129A may promote tumor proliferation and invasion of NSCLC through facilitating the phosphorylation of FAK and upregulated MMP2 and Cyclin D1. Overexpression of FAM129A may be a prognostic predictor in NSCLC patients.
RESUMEN
Expression pattern and biological roles of TRIM22 remains unknown in most human cancers. The present study aims to discover its clinical significance and function in human non-small cell lung cancer (NSCLC). Immunohistochemistry was used to examine TRIM22 expression in 126 cases of NSCLC specimens. TRIM22 protein was upregulated in 70/126 (55.6%) non-small cell lung cancer tissues compared with normal lung tissue. TRIM22 overexpression was associated with advanced TNM stage, positive nodal metastasis and poor prognosis. Plasmid and siRNA transfection were performed in lung cancer cell lines. TRIM22 overexpression promoted proliferation, colony formation and invasion in A549 cells. While its depletion exhibited the opposite effects in H1299 cell line. TRIM22 overexpression promoted cell cycle progression through regulation of cyclin D1, cyclin E and p27. TRIM22 also changed the expression of epithelial to mesenchymal transition (EMT) markers including E-cadherin N-cadherin, Vimentin and Snail. Furthermore, TRIM22 activated PI3K/AKT/GSK3ß/ß-catenin oncogenic signaling pathways. Treatment with PI3K inhibitor LY294002 and ß-catenin siRNA blocked the effects of TRIM22 on EMT in TRIM22-overexpressing cells. In conclusion,TRIM22 serves as an important oncoprotein and a promoter of cell proliferation and invasion through AKT/ GSK3ß/ß-catenin induced EMT in NSCLC.
RESUMEN
Primary tracheobronchial non-Hodgkin lymphoma (NHL) is a rare tracheobronchial tumor that typically presents as an endobronchial mass and/or mucosal infiltration together with lymphadenopathy. Here we report a case of primary tracheobronchial NHL which was confirmed by histopathological analysis of the endobronchial biopsy specimens. We initially could not treat with chemotherapy because the life-threatening obstruction of the bilateral main bronchi caused by NHL. After interventional bronchoscopy involving cryotherapy, electrocautery and argon plasma coagulation to successfully alleviate airway obstruction, we were able to administer chemotherapy, which elicited a good response. This case illustrates that NHL should be considered in the differential diagnosis of central airway obstruction. Interventional bronchoscopy is an effective method to alleviate airway obstruction in primary tracheobronchial NHL and prepare the patient to receive tumor-specific chemotherapy and other treatments.