Abstract
Cancer remains a current active problem of modern medicine, a process during which cell growth and proliferation become uncontrolled. However, the role of autophagy in the oncological processes is counterintuitive and, at the same time, increasingly influential on the formation, development, and response to therapy of oncological diseases. Autophagy is a vital cellular process that removes defective proteins and organelles and supports cellular homeostasis. Autophagy can enhance the ability to form new tumors and suppress this formation in cancer. The dual potential of apoptosis may be the reason for this duality in either promoting or impeding the survival of cancer cells, depending on the situation, including starvation or treatment stress. Furthermore, long non-coding RNA NEAT1, which has been linked to several stages of carcinogenesis and in all forms of the illness, has drawn attention as a major player in cancer biology. NEAT1 is a structural portion of nuclear paraspeckles and has roles in deactivating expression in both transcriptional and post-transcriptional levels. NEAT1 acts in carcinogenesis in numerous ways, comprising interactions with microRNAs, the influence of gene articulation, regulation of epigenetics, and engagement in signalling cascades. In addition, the complexity of NEAT1’s role in cancer occurrence is amplified by its place in regulating cancer stem cells and the tumor microenvironment. NEAT1’s interaction with autophagy further complicates the already complicated function of this RNA in cancer biology. NEAT1 has been linked to autophagy in several types of cancer, influencing autophagy pathways and altering its stress response and tumor cell viability. Understanding the interrelation between NEAT1, autophagy, and cancer will enable practitioners to identify novel treatment targets and approaches to disrupt oncogenic processes, reduce the occurrence of treatment resistance, and increase patient survival rates. Specialized treatment strategies and regimens are thus achievable. In the present review, the authors analyze sophisticated relationship schemes in cancer: The NEAT1 pathway and the process of autophagy.
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