The multifaceted oncogenic role of long intergenic non-coding RNA 01614 in mediating tumor progression and therapeutic resistance: A review.

Abstract

The escalating global burden of human malignancies and frequent therapeutic resistance necessitate the urgent identification of novel molecular targets. Recently, long intergenic non-coding RNA 01614 (LINC01614) has emerged as a pan-cancer oncogenic driver whose functional roles have been experimentally validated across at least ten malignancies. This review comprehensively summarizes the functions, regulatory mechanisms, and clinical significance of LINC01614 in cancer. Functionally, LINC01614 drives multidimensional malignant phenotypes, encompassing epithelial-mesenchymal transition (EMT), metabolic reprogramming, and the immunosuppressive remodeling of the tumor microenvironment (TME). Mechanistically, its highly orchestrated regulatory network initiates with upstream transcriptional activation by factors like STAT1 and SP1, followed by its core function as a competing endogenous RNA (ceRNA) to sequester multiple tumor-suppressive microRNAs. This functionally hyperactivates canonical downstream signaling cascades, including the PI3K/Akt, Wnt/β-catenin, and TGF-β pathways. Clinically, LINC01614 upregulation consistently correlates with aggressive clinicopathological features, potential metastasis, and recalcitrant chemoresistance. By synthesizing these diverse dimensions alongside current translational bottlenecks, this review paper highlights LINC01614 as a highly promising diagnostic biomarker and an actionable therapeutic vulnerability for overcoming drug resistance in precision oncology.