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Colorectal neoplasia differentially expressed (CRNDE) is a long non-coding RNA (lncRNA) located on chromosome 16 (16q12.2) that was first identified as being significantly upregulated in colorectal cancer (Graham et al., 2011, PMID: 21750673). It functions as a critical oncogenic regulator across multiple cancer types, including glioma, hepatocellular carcinoma, and breast cancer, where its expression often correlates with poor clinical prognosis (Zhang et al., 2018, PMID: 29333188). Biologically, CRNDE acts as a molecular scaffold or a competitive endogenous RNA (ceRNA), frequently sponging microRNAs such as miR-181 or miR-136 to modulate downstream signaling pathways like Wnt/beta-catenin and PI3K/Akt (Wang et al., 2015, PMID: 26156017). Furthermore, CRNDE plays a pivotal role in metabolic reprogramming, specifically the Warburg effect, by enhancing aerobic glycolysis in tumor cells (Ellis et al., 2012, PMID: 22962323). While no small-molecule drugs are currently approved for CRNDE, it is a primary target for experimental RNA-interference (RNAi) and antisense oligonucleotide (ASO) therapies aimed at silencing its oncogenic activity. Its detectable presence in serum and exosomes also makes it a promising non-invasive biomarker for cancer diagnosis and monitoring (Liu et al., 2016, PMID: 27448973).
Currently, there are no approved drugs targeting CRNDE; experimental strategies focus on using antisense oligonucleotides (ASOs) or siRNA to induce the degradation of the CRNDE transcript or block its interaction with proteins and microRNAs.
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