RNA-binding proteins (RBPs) represent a large class of post-transcriptional gene expression regulators, driving major stages of RNA metabolism. In humans, more than 1500 RBPs exist and regulate alternative splicing, stability, degradation and localization of hundreds of RNA targets. RBPs act within functional assemblies called ribonucleoprotein granules by establishing highly dynamic interactions with coding and non-coding targets RNAs as well as other proteins. RBPs play a role in a wide range of physiological processes including embryo development, neurogenesis, and metabolism. RBPs require a fine-tuning regulation for the maintenance of cellular equilibrium. Accordingly, alterations in the expression or functions of RBPs significantly contribute to various pathological conditions including cancer.
Despite previously underrated, RBPs have been recognized as a novel class of cancer drivers. Recent pan-cancer studies demonstrate that dysregulation of RBPs occurs ubiquitously in cancer. Interestingly, some RBPs are exclusively dysregulated in single cancer types while others are dysregulated in multiple tumors. RBPs guide most cancer hallmarks, such as stemness, proliferation, cell dissemination, resistance to cell death, immune system evasion. The data from the literature demonstrate that the RNA processing activities of the cancer-driving RBPs are altered, leading to a consequent unbalanced cellular proteome. Aberrant RBPs activity thus creates those cancer vulnerabilities which can be exploited in clinical setting for cancer subtyping and for the identification of novel therapeutic strategies. The clinical use of RBPs is still far from being a concrete possibility due to the many molecular and technical issues that remain unsolved.
This research topic aims to collect the most recent advancements in RBPs-related translational cancer research. We welcome high-quality, original research articles and review articles focusing on improving the current knowledge in the RBPs field and introducing novel applications in cancer biomarkers and therapy related to specific cancers, clinical subgroups or pan-cancer studies. The most relevant papers will be those which focus in the key areas below:
1) Mechanisms governing the altered RBPs expression in cancer. Contexts could comprise, but not limited to: genetic alterations, epigenetic changes, post-transcriptional mechanisms including non-coding RNA-mediated processes, post-translational modifications.
2) Cellular and molecular functions of RBPs in the aberrant post-transcriptional control of gene expression. Contexts could include, but not limited to: detection of RBP–RNA interactions, global-scale analysis for RBPs targets identification, interaction between RBPs and the tumor microenvironment.
3) RBPs and RBPs-related interactors as biomarkers of prognosis/diagnosis/response to treatment.
4) Approaches to target RBPs with the specific aim to treat cancer or understand cancer biology.
RNA-binding proteins (RBPs) represent a large class of post-transcriptional gene expression regulators, driving major stages of RNA metabolism. In humans, more than 1500 RBPs exist and regulate alternative splicing, stability, degradation and localization of hundreds of RNA targets. RBPs act within functional assemblies called ribonucleoprotein granules by establishing highly dynamic interactions with coding and non-coding targets RNAs as well as other proteins. RBPs play a role in a wide range of physiological processes including embryo development, neurogenesis, and metabolism. RBPs require a fine-tuning regulation for the maintenance of cellular equilibrium. Accordingly, alterations in the expression or functions of RBPs significantly contribute to various pathological conditions including cancer.
Despite previously underrated, RBPs have been recognized as a novel class of cancer drivers. Recent pan-cancer studies demonstrate that dysregulation of RBPs occurs ubiquitously in cancer. Interestingly, some RBPs are exclusively dysregulated in single cancer types while others are dysregulated in multiple tumors. RBPs guide most cancer hallmarks, such as stemness, proliferation, cell dissemination, resistance to cell death, immune system evasion. The data from the literature demonstrate that the RNA processing activities of the cancer-driving RBPs are altered, leading to a consequent unbalanced cellular proteome. Aberrant RBPs activity thus creates those cancer vulnerabilities which can be exploited in clinical setting for cancer subtyping and for the identification of novel therapeutic strategies. The clinical use of RBPs is still far from being a concrete possibility due to the many molecular and technical issues that remain unsolved.
This research topic aims to collect the most recent advancements in RBPs-related translational cancer research. We welcome high-quality, original research articles and review articles focusing on improving the current knowledge in the RBPs field and introducing novel applications in cancer biomarkers and therapy related to specific cancers, clinical subgroups or pan-cancer studies. The most relevant papers will be those which focus in the key areas below:
1) Mechanisms governing the altered RBPs expression in cancer. Contexts could comprise, but not limited to: genetic alterations, epigenetic changes, post-transcriptional mechanisms including non-coding RNA-mediated processes, post-translational modifications.
2) Cellular and molecular functions of RBPs in the aberrant post-transcriptional control of gene expression. Contexts could include, but not limited to: detection of RBP–RNA interactions, global-scale analysis for RBPs targets identification, interaction between RBPs and the tumor microenvironment.
3) RBPs and RBPs-related interactors as biomarkers of prognosis/diagnosis/response to treatment.
4) Approaches to target RBPs with the specific aim to treat cancer or understand cancer biology.
