review · Cells
Cancer remains a leading cause of global mortality, with advanced stages showing limited response to existing treatments. Researchers are reanalysing molecular mechanisms, particularly autophagy, to identify potential therapeutic routes. Autophagy is a conserved catabolic process that degrades damaged organelles and protein aggregates to maintain cellular balance. In cancer, autophagy plays dual roles, acting either to promote or suppress tumours depending on disease stage and grade. Notably, it supports tumour survival and nutrient recycling under hypoxic and nutrient-poor conditions. Long non-coding RNAs have emerged as critical regulators of autophagic gene expression. By sequestering autophagy-related microRNAs, long non-coding RNAs modulate major hallmarks of cancer progression, including cell proliferation, survival, epithelial to mesenchymal transition, migration, invasion, angiogenesis, and metastasis across various cancer types.
Advanced cancers frequently result in poor clinical outcomes, necessitating the identification of new treatment targets. Understanding how long non-coding RNAs regulate autophagy reveals the mechanisms cancer cells use to survive stressful environments and spread. This insight is essential for researchers working to design therapies that can disrupt tumour maintenance and overcome treatment resistance.
This work represents early-stage basic research reviewing molecular mechanisms. The described pathways could eventually assist oncology drug discovery teams in identifying long non-coding RNAs or autophagy pathways as drug targets. However, the abstract describes conceptual and mechanistic relationships rather than applied technologies, meaning any real-world clinical or commercial application remains at a very early, exploratory stage.
AI-generated from the published abstract. Always read the original work before citing.
Cancer has become a global health hazard accounting for 10 million deaths in the year 2020. Although different treatment approaches have increased patient overall survival, treatment for advanced stages still suffers from poor clinical outcomes. The ever-increasing prevalence of cancer has led to a reanalysis of cellular and molecular events in the hope to identify and develop a cure for this multigenic disease. Autophagy, an evolutionary conserved catabolic process, eliminates protein aggregates and damaged organelles to maintain cellular homeostasis. Accumulating evidence has implicated the deregulation of autophagic pathways to be associated with various hallmarks of cancer. Autophagy exhibits both tumor-promoting and suppressive effects based on the tumor stage and grades. Majorly, it maintains the cancer microenvironment homeostasis by promoting viability and nutrient recycling under hypoxic and nutrient-deprived conditions. Recent investigations have discovered long non-coding RNAs (lncRNAs) as master regulators of autophagic gene expression. lncRNAs, by sequestering autophagy-related microRNAs, have been known to modulate various hallmarks of cancer, such as survival, proliferation, EMT, migration, invasion, angiogenesis, and metastasis. This review delineates the mechanistic role of various lncRNAs involved in modulating autophagy and their related proteins in different cancers.
This page summarises published work. The authoritative version sits with the publisher.
DOI: 10.3390/cells12050810
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