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The protein, tripartite motif containing 24 (TRIM24) is a member of the TRIM protein family, and acts as a critical co‐regulator of multiple nuclear receptors. TRIM24 is dysregulated in many cancers, including colorectal carcinoma. However, its biological functions and molecular mechanisms with respect to colorectal carcinoma are still largely unknown. In the current study, we found that TRIM24 promotes YAP signaling for driving cell proliferation in colorectal cancer. TRIM24 was significantly upregulated in colorectal carcinoma, and its expression was negatively correlated with the survival of patients. Depletion of TRIM24 impaired the ability of the cancer cells to proliferate and form colonies. Furthermore, this study also revealed the mechanism underlying the recruitment of TRIM24 by the DANCR/KAT6A complex, which is bound to acetylated lysine 23 of histone H3 (H3K23), resulting in binding to the YAP promoter and activation of YAP transcription that ultimately enhances the proliferation of colorectal cancer cells. Our results revealed a novel mechanism involving TRIM24‐YAP signaling for the regulation of colorectal cancer. We also identified TRIM24 as a potential therapeutic molecule for targeting colorectal cancer. [ABSTRACT FROM AUTHOR]

Recent studies have demonstrated that long non-coding RNAs (lncRNAs) play critical roles in cancer development and progression. However, the mechanism by which lncRNAs contribute to colorectal cancer remains unclear. In this study, we identified the lncRNA, DANCR , which was upregulated in colorectal cancer. The upregulation of DANCR expression was associated with shorter patient survival time. DANCR depletion decreased cell proliferation, cell cycle progression, and tumorigenesis in a subcutaneous mouse xenograft model system. We further demonstrated that DANCR bound with lysine acetyltransferase 6A. This binding was essential for KAT6A acetyltransferase activity and thus, it influenced the expression of KAT6A target genes. Our data indicated that DANCR functions as an oncogenic lncRNA that promotes tumor development and progression. Therefore, DANCR may be a target molecule for colorectal cancer treatment. • In the present study, we observed that DANCR was upregulated in colorectal cancer compared with normal colorectal tissues and that it predicted poor patient survival. • DANCR promoted colorectal cancer cell proliferation and cell cycle arrest by activating the H3K23 acetyltransferase, KAT6A, and by activating cell cycle-related proteins. • Collectively, our results identified a new regulatory mechanism by which DANCR promotes colorectal cancer progression, providing a potential therapeutic target and prognostic factor for colorectal cancer. [ABSTRACT FROM AUTHOR]