From code to cancer: CircRNAs and lncRNAs regulate kinesin functions in tumorigenesis.

There has been a paradigm shift in the pathogenesis mechanisms of cancer over the past few decades in oncology, whereby the regulators of tumorigenesis are non-coding RNAs (ncRNAs). Circular RNAs (circRNAs) and long non-coding RNAs (lncRNAs) have also recently been of great interest due to their roles as regulatory molecules in pathological processes, including cancer. These regulatory molecules operate partially by interfering with kinesin superfamily proteins (KIFs)-cellular molecular motors implicated in the transport phenomena within a cell and related processes, including post-mitotic and basic cell functions. Cumulative evidence shows that ncRNA-KIF networks operate through independent mechanistic pathways. In most cases, circRNAs function as competitive endogenous RNAs by sequestering microRNAs and modulating the indirect pathway of KIF expression. lnRNAs can bind protein or mRNA of KIF directly and modify its function or stability. Briefly, they all share a broad range of cancer hallmarks such as heightened proliferative signaling pathways, drug resistance, and invasion and metastasis. Several ncRNA-KIF axes are tissue-specific in the three cancers, namely glioblastoma, breast cancer, and colorectal carcinoma, and thus are also potential therapeutic targets, along with biomarkers. The clinical relevance of this finding is that strong ncRNA-KIF signatures would likely allow for the early detection of cancer with a favorable prognosis; such interactions would unveil novel therapies, particularly in therapy-refractory tumors. For example, inhibiting oncogenic ncRNA-KIF networks or restoring tumor-suppressive ones would be related to all existing methods. With advancing science, a progressively more evolved view of such regulatory networks will reveal increasingly complex layers in cancer biology and identify novel targets for RNA-based therapies. Such advances in new knowledge underscore the importance of extending current research into ncRNA-KIF interactions and their translational relevance to precision oncology.