ABSTRACT
Malignant tumors, whose occurrence and development are related to a variety of RNA transporter proteins, seriously affect human health and quality of life. Under normal circumstances, RNA transport proteins help RNA shuttle between nucleus and cytoplasm and their precise localization, effectively coupling the life activities in the nucleus and cytoplasm. During the process of tumorigenesis and progression, the expression and localization of some RNA transporters are abnormal or dysfunctional, which can change the subcellular localization, expression level, transport efficiency of downstream key RNA molecules, and the decay rate of cytoplasmic mRNA, and affect the proliferation, invasion and metastasis of tumors. This paper mainly reviews RNA transport proteins and their expression changes and regulation in tumors.
ABSTRACT
Malignant tumors, whose occurrence and development are related to a variety of RNA transporter proteins, seriously affect human health and quality of life. Under normal circumstances, RNA transport proteins help RNA shuttle between nucleus and cytoplasm and their precise localization, effectively coupling the life activities in the nucleus and cytoplasm. During the process of tumorigenesis and progression, the expression and localization of some RNA transporters are abnormal or dysfunctional, which can change the subcellular localization, expression level, transport efficiency of downstream key RNA molecules, and the decay rate of cytoplasmic mRNA, and affect the proliferation, invasion and metastasis of tumors. This paper mainly reviews RNA transport proteins and their expression changes and regulation in tumors.
ABSTRACT
Alzheimer's disease (AD) is a neurodegenerative disorder represented by the accumulation of intracellular tau protein and extracellular deposits of amyloid-ß (Aß) in the brain. The gene sortilin 1 (SORT1) has previously been associated with cardiovascular disease in gene association studies. It has also been proposed to be involved in AD pathogenesis through facilitating Aß clearance by binding apoE/Aß complexes prior to cellular uptake. However, the neuropathological role of SORT1 in AD is not fully understood. To evaluate the associations between gene variants of SORT1 and risk of AD, we performed genetic analyses in a Swedish case-control cohort. Ten single nucleotide polymorphisms (SNPs), covering the whole SORT1 gene, were selected and genotyped in 620 AD patients and 1107 controls. The SNP rs17646665, located in a non-coding region of the SORT1 gene, remained significantly associated with decreased risk of AD after multiple testing (pcâ=â0.0061). In addition, other SNPs were found to be nominally associated with risk of AD, as well as altered cognitive function and the CSF biomarker Aß42, but these associations did not survive correction for multiple testing. The fact that SORT1 has been strongly associated with risk of cardiovascular disease is intriguing as cardiovascular disease is also regarded as a risk factor for AD. Finally, increased knowledge about SORT1 function has a potential to increase our understanding of APOE, the strongest risk factor for AD.
