A growing number of non-coding RNAs (lncRNAs) with a length of 200 nucleotides or more affect gene expression and participate in physiological processes like differentiation, death, and proliferation. Through a variety of methods, the development of cancer, including solid tumors and blood malignancies, has been related to the aberrant expression of lncRNAs. These mechanisms include microRNA binding competition, chromatin structural alterations, precursor mRNA processing modifications, and transcriptional and post-transcriptional gene expression regulation [22], [26], [63]. This review focuses on the critical function that the long non-coding RNA Colorectal Neoplasia Differentially Expressed (CRNDE) plays in the advancement of cancer. The term "long non-coding RNA," or "lncRNA," has its roots in the early 21st century. The 2001 scientific paper and the Nature article entirely depicted the human genome, which covered 96% and 100% of the genome, respectively [70], [92]. In 2003, the human genome's final sequence was published. Only a small amount (1.2%) of human genetic material was found to encode proteins, which surprised scientists. The remaining 99% is non-coding DNA, with 24% intron DNA and 75% intergenic DNA [7], [38].

Over 200 base pairs is the length of a long RNA molecule or lncRNA. Transcribing these molecules are RNA polymerase II, III, IV, and V. Except those produced from larger molecules like intronic and circRNA, most lncRNAs include a 5′ cap that aids in stabilizing their RNA structure [85]. Polyadenylation at the 3′ end of lncRNA plays a role in structural stabilization, but its impact is limited to specific regions. Biomorphic lncRNAs can have either a polyadenylated 3′ end or lack it [4], [38]. Splicing generates diverse long non-coding RNAs through the presence of multiple exon segments. Various types of something can play significant roles in clinical settings. Non-coding ribonucleic acids have genes resembling protein-coding genes, but their expression of lncRNA genes is significantly lower. The structure of lncRNA gene promoters and enhancers, particularly with epigenetic histone changes, can lead to reduced severity in transcription and lower stability compared to mRNA. The strength of lncRNA is determined by its type. Intron and promoter-related lncRNAs have lower stability than intergenic, antisense, or end-related 3′ UTRs [3].

On chromosome 16.q12.2, there are several variations of the CRNDE gene. Ten of these variants are listed in the NCBI AceView database. Some elements (a, b, c, g, h, i, j) are spliced together entirely, while other elements (e, f, l) are spliced partially [64]. These variations can be found in many cellular constituents and tissues. Cancer cells commonly exhibit g and b. Whereas partially spliced transcripts are primarily found in the nucleus, fully spliced transcripts are detected in the cytoplasm [65]. This function is most noticeable in cell lines that have high expression of CRNDE, such as NB4 (acute promyelocytic leukemia cell line), HT29 (human colorectal adenocarcinoma cell line), and HCT116 (human colorectal carcinoma cell line). A particular version, CRNDE-b, results in the production of CRNDEP, a brief nucleic acid fragment that is strongly expressed in tissues that proliferate quickly, like intestinal crypts and sperm cells [21], [66]. A thorough grasp of CRNDE's function in cancer progression is essential, as this has significant ramifications for both basic research and therapeutic applications. Even though CRNDE dysregulation in cancer has been proven, little is known about how it operates, especially in the epithelial-mesenchymal transition (EMT) process. By assembling the corpus of research already in existence and shedding light on the intricate biochemical pathways that CRNDE mediates and which are accountable for the development of cancer, this review aims to fill this knowledge gap. The conclusions drawn from this study may open the door to creating novel cancer treatment strategies and diagnostic instruments.