Roles of long-non-coding RNAs in cancer therapy through the PI3K/Akt signalling pathway
Katherine Ting-Wei Lee, Vinod Gopalan and Alfred King-yin Lam
Cancer Molecular Pathology, School of Medicine, Griffith University, Gold Coast, Queensland, Australia
Offprint requests to: Prof. Alfred K. Lam, School of Medicine and Menzies Health Institute Queensland, Griffith University, Gold Coast, Queensland 4222, Australia. e-mail: a.lam@griffith.edu.au
Summary. The vital need for Akt in maintaining basic cellular function has highlighted its importance in carcinogenesis. Unfortunately, Akt inhibitor development outcome has remained poor, as most of them have failed to show significant clinical benefit to cancer patients during the clinical trials. Recently, a new class of non-coding RNAs, known as long non-coding RNAs (lncRNAs), which show high tissue specificity, have demonstrated great influence in cancer progression and/or cancer inhibition. As both Akt signalling pathways and lncRNAs play such innate roles in carcinogenesis, identifying the specific roles that these lncRNAs play within this pathway may represent a novel research avenue for developing Akt inhibitors with better therapeutic properties. In addition, understanding the diverse mechanism by which lncRNAs regulate gene expression can assist in deciphering the fundamentals of carcinogenesis. The focus of interest should be on the lncRNAs, which affect Akt and finding the link between lncRNAs and Akt pathways associated with carcinogenesis. LncRNAs within the Akt pathways could affect multiple pathways in a particular cancer type, which ultimately creates an intricate web of connections between the pathways. In summary, lncRNAs have tremendous potential in cancer diagnosis, assessing cancer patient prognosis and in developing new therapeutic options for patients with resistance to current cancer therapies. Thus, understanding how lncRNAs influence the Akt pathway is essential for the development of novel and effective cancer therapies. Histol Histopathol 34, 593-609 (2019)
Key words: Akt, LncRNAs, Cancer, Resistance, CeRNA, PI3K/Akt
DOI: 10.14670/HH-18-081