Doublecortin-like kinase 1 (DCLK1) mRNA (DCLK1 mRNA)

Doublecortin-like kinase 1 (DCLK1) mRNA encodes a microtubule-associated protein kinase that is a prominent marker for cancer stem cells (CSCs) in several solid tumors, most notably colorectal and pancreatic cancers [1][2]. The DCLK1 protein is characterized by two N-terminal doublecortin domains and a C-terminal serine/threonine kinase domain, which together regulate microtubule polymerization and signal transduction pathways essential for cell migration and survival [3][4]. In the context of oncology, DCLK1 mRNA expression is often upregulated and correlates with poor prognosis, as it promotes the epithelial-mesenchymal transition (EMT) and enhances the self-renewal capacity of tumor-initiating cells [5]. A key therapeutic advantage of targeting DCLK1 mRNA is its selective expression in CSCs compared to normal intestinal or pancreatic stem cells, potentially minimizing toxicity to healthy tissues [6]. Therapeutic strategies focusing on the mRNA include the use of small interfering RNAs (siRNAs) and antisense oligonucleotides designed to trigger the degradation of the transcript, thereby depleting the DCLK1 protein [7]. Preclinical studies using nanoparticle-delivered siRNAs, such as COH203, have shown success in inhibiting tumor growth and sensitizing cancer cells to conventional chemotherapy [8]. Despite its promise, challenges remain regarding the efficient delivery of RNA-based therapeutics to the tumor microenvironment and the potential for off-target effects within the RNAi pathway [9].

Other names

DCAMKL1 mRNADoublecortin and CaM kinase-like 1 mRNADCLK mRNADoublecortin-like and CAM kinase-like 1 mRNA

RNA interference (RNAi) mediated degradation of DCLK1 mRNA, leading to the inhibition of DCLK1 protein synthesis.