circ‑FNTA accelerates proliferation and invasion of bladder cancer

Abstract

Role of circ-FNTA in the progression of bladder cancer (BCa) and its underlying mechanism were investigated. circ-FNTA level in BCa tissues and cell lines was detected. The prognostic potential of circ-FNTA was assessed by Kaplan-Meier methods and the proliferative and invasive abilities of BCa influenced by circ-FNTA were explored. Through dual-luciferase reporter gene assay, miRNA-451a, the target of circ-FNTA and the target gene of miRNA-451a, S1PR3 were determined. circ-FNTA was upregulated in BCa, especially in invasive BCa. High level of circ-FNTA indicated worse prognosis in BCa patients. Silence of circ-FNTA attenuated the proliferative and invasive abilities of T24 and UM-UC-3 cells. miRNA-451a was verified to be the target of circ-FNTA, which was downregulated in BCa cells. circ-FNTA negatively regulated the expression level of miRNA-451a. Moreover, S1PR3 was the downstream gene of miRNA-451a. Overexpression of miRNA-451a downregulated S1PR3 level in BCa cells. circ-FNTA accelerates the proliferative and invasive abilities of BCa through targeting miRNA-451a/S1PR3 axis, and indicates a poor prognosis of BCa patients.

Enriched transcriptome analysis of laser capture microdissected populations of single cells to investigate intracellular heterogeneity in immunostained FFPE sections

“…The top significantly upregulated gene in the PR-low cell population ( Fig. 4 a) is Farnesyltransferase (FNTA), a central regulator of pro-tumorigenic and pro-metastatic GTPases signaling through regulating GTPases translocation to the plasma membrane [49] , [50] , [51] . Another top upregulated gene in PR-low cells is SPOUT Domain Containing Methyltransferase 1 (C9orf114; also known as SPOUT1), a methyltransferase and kinetochore-associated protein involved chromosomes alignment, mitotic spindle assembly and cell division [52] .…”

Identifying common transcriptome signatures of cancer by interpreting deep learning models

“…Interestingly, several of these genes that are not listed as COSMIC oncogenes still display tumorigenic characteristics. A few examples include DYNC1H1 (Gong et al, 2019), WSB1 (Kim et al, 2016;Cao et al, 2015;Kim et al, 2015), RUFY3 (Xie et al, 2017;Wang et al, 2015), DOCK5 (Frank et al, 2016), MYSM1 , DSE (Liao et al, 2018), DCUN1D5 (Bommeljé et al, 2013;Guo et al, 2012), SARNP (Kang et al, 2019) and FNTA (Tian et al, 2019;Chen et al, 2020a), which can all promote cell proliferation or transformation, at least in some conditions. Likewise, we have identified splice junctions in cancer that deviate from normal tissues in functional domains implicated in cancer signaling, such as PKC-like (Garg et al, 2013), DEAD-like (Fuller-Pace, 2013) and RING (Lipkowitz & Weissman, 2011) domains, in genes associated with cancer, such as CSNK2A1, CSNK2A2, RIOK1, PRKDC, TYK2, PAK1 and IRAK1, for which gene expression and posttranslational modifications act as mechanisms for cancer progression (Zhang et al, 2019;Hong et al, 2018;Gray et al, 2014;Wöss et al, 2019;Ye & Field, 2012;Cheng et al, 2018).…”

Circular RNAs and Drug Resistance in Genitourinary Cancers: A Literature Review

“…In addition, miRNA-451a is downregulated by circ-FNTA, and the effect of miRNA-451a is to reduce the level of Sphingosine-1-phosphate Receptor 3 (S1PR3). The increase of circ-FNTA promotes the progression and chemo-resistance of BCa [ 81 ].…”