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https://www.selleckchem.com/products/inx-315.html To study the effect and potential mechanism of LKB1 on non-small cell lung cancer (NSCLC) A549 cells. A549 cells were divided into control group, LKB1 negative control (NC) group, LKB1 group, ERK inhibitor group and LKB1 + ERK activator group. Cell proliferation and apoptosis were detected by cell counting kit (CCK-8) assay and flow cytometry, respectively. Transwell assay was used to analyze the invasion ability of A549 cells. The expression of apoptosis and ERK signaling pathway-related proteins were studied by Western blot. Furthermore, a nude mouse xenograft model was constructed and treated with LKB1, ERK inhibitor and activator, respectively. The tumor volume and tumor weight were measured. Immunohistochemistry was used to test the expression of Ki-67 protein in tumor tissues, and TUNEL staining was used to test the apoptosis. Moreover, Western blot was used to detect ERK signaling pathway-related proteins in tumor tissues. Compared with control and NC groups, cell proliferation and invasion were inhibited in ERK inhibitor and LKB1 groups, while apoptosis and apoptosis-related proteins were increased (p < 0.05). Further study showed that ERK activator can reverse the effect of LKB1 in A549 cells. In nude mice, ERK inhibitor and LKB1 can reduce cell tumorigenicity and inhibit proliferation. Apoptosis was increased by ERK inhibitor and LKB1 treatment. Western blot showed that LKB1 and ERK inhibitor could reduce the protein expression of p-ERK1/2. However, the indicators above were the opposite in the ERK activator group. LKB1 overexpression can inhibit proliferation and promote apoptosis of NSCLC A549 cells, and its mechanism may be related to inhibition of the ERK signaling pathway. LKB1 overexpression can inhibit proliferation and promote apoptosis of NSCLC A549 cells, and its mechanism may be related to inhibition of the ERK signaling pathway. DNA methylation is known to play an important role in myelodysplast

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