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https://www.selleckchem.com/products/iclepertin.html We observed that circUGGT2 and RAB1A were upregulated while miR-526b-5p was downregulated in HCC tissues and cells. CircUGGT2 silencing suppressed tumor growth in vivo and curbed proliferation, colony formation, cell cycle progression, migration, and invasion of HCC cells in vitro. Mechanically, circUGGT2 regulated RAB1A expression via competitively binding to miR-526b-5p. Also, the inhibitory influence of circUGGT2 silencing on the malignancy of HCC cells was overturned by miR-526b-5p inhibitor. Furthermore, RAB1A overexpression reversed the suppressive influence of miR-526b-5p mimic on the malignancy of HCC cells. CircUGGT2 silencing inhibited HCC development via modulating the miR-526b-5p/RAB1A axis, providing a possible target for HCC treatment. CircUGGT2 silencing inhibited HCC development via modulating the miR-526b-5p/RAB1A axis, providing a possible target for HCC treatment. Colorectal cancer is one of the most common malignant tumors worldwide. ASXL2 is an enhancer of the trithorax and polycomb genes, which have been proven to act in many tumor types. The role of ASXL2 in the occurrence and development of tumors has been extensively studied in recent years. However, the relationship between ASXL2 and the prognosis of CRC is still unclear. In this study, quantitative real-time polymerase chain reaction (qRT-PCR), Western blot analysis and immunohistochemistry (IHC) were used to examine the expression of ASXL2 in CRC tissues. Cells were transfected with siRNAs or lentivirus to regulate the expression of ASXL2. The effects of ASXL2 on the proliferation of CRC cells were determined by CCK8 assay. This study demonstrated that ASXL2 was significantly more highly expressed in CRC specimens than in normal adjacent tissues. The upregulation of ASXL2 was related to advanced clinical stage. Patients who exhibited high expression levels of ASXL2 had poorer overall survival, whereas those with low expression of ASXL2

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