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Background: Effective identification and development of new molecular methods for the diagnosis, treatment and prognosis of lung adenocarcinoma (LUAD) remains an urgent clinical need. DNA methylation patterns at cytosine bases in the genome are closely related to gene expression, and abnormal DNA methylation is frequently observed in various cancers. The ten-eleven translocation (TET) enzymes oxidize 5-methylcytosine (5mC) and promote locus-specific DNA methylation reversal. This study aimed to explore the role of the TET2 protein and its downstream effector, 5-hmC/5-mC DNA modification, in LUAD progression. Methods: The expression of TET2 was analysed by real-time PCR, Western blotting and immunohistochemistry. The 5-hmC DNA content was determined by a colorimetric kit. Activation of the cGAS-STING signalling pathway was evaluated by Western blotting. CCK-8, wound healing and Transwell assays were performed to evaluate the effect of TET2 on cell proliferation, migration and invasion abilities. A xenograft model was used to analyse the effect of TET2 on the tumorigenic ability of A549 cells. Results: TET2 overexpression decreased proliferation and metastasis of A549 and H1975 cells in vitro and in vivo. However, TET2 knockdown dramatically enhanced the proliferation, migration and invasion of A549 and H1975 cells. Mechanistically, activation of the cGAS-STING signalling pathway is critical for the TET2-mediated suppression of LUAD cell tumorigenesis and metastasis. Conclusion: In this study, we demonstrate a tumour suppressor role of TET2 in LUAD, providing new potential molecular therapeutic targets and clinical therapies for patients with non-small cell lung cancer. [ABSTRACT FROM AUTHOR]

Background: Mikania micrantha is a vine with strong invasion ability, and its strong sexual reproduction ability is not only the main factor of harm, but also a serious obstacle to control. M. micrantha spreads mainly through seed production. Therefore, inhibiting the flowering and seed production of M. micrantha is an effective strategy to prevent from continuing to spread. Result: The flowering number of M. micrantha is different at different altitudes. A total of 67.01 Gb of clean data were obtained from nine cDNA libraries, and more than 83.47% of the clean reads were mapped to the reference genome. In total, 5878 and 7686 significantly differentially expressed genes (DEGs) were found in E2 vs. E9 and E13 vs. E9, respectively. Based on the background annotation and gene expression, some candidate genes related to the flowering pathway were initially screened, and their expression levels in the three different altitudes in flower bud differentiation showed the same trend. That is, at an altitude of 1300 m, the flower integration gene and flower meristem gene were downregulated (such as SOC1 and AP1), and the flowering inhibition gene was upregulated (such as FRI and SVP). Additionally, the results showed that there were many DEGs involved in the hormone signal transduction pathway in the flower bud differentiation of M. micrantha at different altitudes. Conclusions: Our results provide abundant sequence resources for clarifying the underlying mechanisms of flower bud differentiation and mining the key factors inhibiting the flowering and seed production of M. micrantha to provide technical support for the discovery of an efficient control method. [ABSTRACT FROM AUTHOR]