Cancer susceptibility candidate 11 (non-protein coding) (CASC11)

Cancer susceptibility candidate 11 (CASC11) is a long non-coding RNA (lncRNA) located on chromosome 8q24.21 that does not encode a protein but exerts extensive regulatory control over gene expression and cell signaling[1][3][5]. CASC11 is found to be upregulated in several types of malignant tumors, including prostate, colorectal, liver, and gastric cancers, where its high expression is generally associated with poor prognosis, advanced clinicopathological features, and increased metastasis[1][3][5][7]. CASC11 promotes cancer progression by regulating cell proliferation, migration, invasion, cell cycle progression (notably G1/S transition), and apoptosis. Mechanistically, CASC11 acts as a competitive endogenous RNA (ceRNA), sequestering various microRNAs (such as miR-150, miR-646, miR-381-3p, and others), interacts with chromatin modifiers and transcription factors (including c-Myc, STAT3, and YBX1), and modulates key oncogenic signaling including Wnt/β-catenin, PI3K/AKT, p53 pathway, and EMT[1][3][5]. CASC11 expression is regulated by several oncogenic transcription factors and serves as a potential diagnostic and prognostic biomarker for cancer diagnosis, progression, and therapy monitoring; it is detectable in both tissues and plasma. Due to its pivotal oncogenic role and involvement in multiple regulatory networks, CASC11 is being investigated as a therapeutic target in oncology[1][3][5]. No currently approved drugs are known to specifically target CASC11 directly. Safety and specificity concerns arise from the broad regulatory actions of lncRNAs and their potential to affect numerous cellular pathways in both malignant and normal tissues[5].

Other names

TCONS_00014535LINC00990CARLo-7ENST00000518376MYMLRLong intergenic non-protein coding RNA 990MYC‐modulating lncRNACARLO7MYC-modulating lncRNA

Acts as a competitive endogenous RNA (ceRNA), sponges microRNAs to derepress oncogene targets, interacts with proteins/transcription factors (e.g., YBX1, c-Myc, STAT3, hnRNP-K), modulates signaling pathways (Wnt/β-catenin, PI3K/AKT, p53 pathway, EMT)