Relationship between Sphk1/S1P and microRNAs in human cancers

Abstract

Sphingosine kinases type 1 (SphK1) is a key enzyme in the phosphorylation of sphingosine to sphingosine 1‐phosphate (S1P). Different abnormalities in SphK1 functions may correspond with poor prognosis in various cancers. Additionally, upregulated SphK1/S1P could promote cancer cell proliferation, angiogenesis, mobility, invasion, and metastasis. MicroRNAs as conserved small noncoding RNAs play major roles in cancer initiation, progression, metastasis, etc. Their posttranscriptionally mechanisms could affect the development of cancer growth or tumorigenesis suppression. The growing number of studies has described that various microRNAs can be regulated by SphK1, and its expression level can also be regulated by microRNAs. In this review, the relationship of SphK1 and microRNA functions and their interaction in human malignancies have been discussed. Based on them novel treatment strategies can be introduced.

RETRACTED ARTICLE: Long non-coding RNA 00960 promoted the aggressiveness of lung adenocarcinoma via the miR-124a/SphK1 axis

“…As a widely occurring secondary messenger molecule, S1P is a vital regulator of various diseases, including cancer, atherosclerosis, fibrosis, and multiple sclerosis [ 29–31 ]. Szasz et al [ 32 ] have demonstrated that overexpression of SphK1 predicts poor overall survival [ 33 ]. However, the putative association between miR-124a and the Sphk1/S1P pathway needs to be comprehensively elucidated.…”

Identification of natural products as dual sphingosine kinase-1 and programmed cell-death 1-inhibitors by virtual screening and molecular dynamics simulation

“…Sphk1 can induce T cell failure through excessive S1P in extracellular vesicles of the tumor microenvironment. The study demonstrate that down regulation S1P lead to the increase of CD8 + T cells and decrease of Treg cells in the tumor microenvironment [6,7] . S1P also upregulates the expression of PD-L1 through Early 2 factor transcription factor 1 (E2F1) [8] .…”

“…Sphk1 catalyzes the phosphorylates of sphingosine to generate sphingosine-1-phosphate (S1P). Sphk1/S1P signal pathway not only influences tumor cells growth, proliferation, survival and angiogenesis, but also regulates immunotherapy [5,6] . Sphk1 can induce T cell failure through excessive S1P in extracellular vesicles of the tumor microenvironment.…”

A Convergent Functional Genomics Analysis to Identify Biological Regulators Mediating Effects of Creatine Supplementation

“…These post-transcriptional gene regulators open a new field of research regarding the therapeutic role of CrM supplementation on health-related conditions. It needs to be noted that the osmosensing activation of MAPK via Sphk1/S1P is related to several miRNAs [ 142 ], as well as the notion that the effect of Cr on focal adhesion kinase [ 38 , 70 ] ( Figure A1 ) might control muscle cell differentiation through a small set of miRNAs that are connected to the focal adhesion signaling during muscle regeneration, as was reported recently [ 143 ]. Further experimental validation is warranted in the future.…”