Anti-MTA1 (aa 601-700) polyclonal antibody

Objective This study is aimed to explore the role of miR-543 in non-small cell lung cancer (NSCLC), and verify whether miR-543 targets metastasis associated protein 1 (MTA1) to affect tumorigenesis and angiogenesis in NSCLC. Methods Firstly, miR-543 mimic and inhibitor were transfected into A549 cells and H1299 cells. The cells proliferation was tested by MTT and clone formation. The cells apoptosis was analyzed by cytometry. Tube formation assay was used to measure the vascularization of cells. qRT-PCR and Western Blot were used to measure the MTA1 expression. Dual-luciferase assay was used to analyze whether miR-543 targets MTA1. Secondly, MTA1 mimic and inhibitor were transfected into cells to analyze the effect of MTA1 on proliferation and angiogenesis in NSCLC cells. Lastly, the nude mice were used to verify the effect of miR-543 on tumorigenesis and angiogeneisis in NSCLC via modulating MATA1. Results miR-543 overexpression could apparently promote cells proliferation and angiogeneisis in NSCLC cells. Meanwhile, the MTA1 expression was increased after transfecting miR-543 mimic. Dual luciferase reporter assay revealed MTA1 was a downstream target of miR-543. Further studies showed that inhibition of MTA1 weakened the role of miR-543 overexpression in NSCLC cells. Vivo experiments revealed that miR-543 promoted cells proliferation and angiogenesis in tumor tissues via modulating MTA1. Conclusion miR-543 could target MTA1 to promote tumorigenesis and angiogenesis in NSCLC via targeting MTA1.

Background: Liver cancer is the third leading cause of tumor-related deaths worldwide. Stomatin-like protein 2 (STOML2) is obviously upregulated in various tumors. In this study, we explored the potential roles and mechanisms of si-STOML2 in the migration and invasion of human hepatoma LM3 cells. Material/Methods: The expression levels of STOML2 in tissues and cells were separately analyzed with quantitative real-time PCR (qRT-PCR) and Western blotting. The viability, migration, and invasion of cells were assessed by cell counting kit-8 (CCK-8), wound healing, and transwell analysis, respectively. The mRNA and protein levels of various factors were separately measured using qRT-PCR and Western blotting. Correlation analysis between the expression of STOML2 and the clinicopathological features of liver cancer patients was evaluated using the chi-square test. Results: Surprisingly, our results showed that STOML2 was upregulated in liver cancer tissue and cells, and this upregulation was linked to tumor size, histologic grade, and metastasis, but was not associated with sex, age, or TNM stage. The knockdown of STOML2 significantly repressed the viability, migration, and invasion of LM3 cells. We also observed that silencing STOML2 markedly downregulated the expression levels of matrix metalloproteinase-2 (MMP-2), MMP-9, metastatic tumor antigen 1 (MTA1), and nuclear factor kappa B (NE-kappa B), and upregulated levels of E-cadherin, tissue inhibitor of metalloproteinases 2 (TIMP2), and the inhibitor of kappa B (I kappa B). Conclusions: STOML2 has a vital role in the progression of liver cancer. STOML2 silencing in LM3 cells obviously repressed the abilities of migration and invasion via suppressing the NE-kappa B pathway.