This study suggests that speckle-type POZ protein (SPOP) may be a tumor suppressor gene and its prognostic value in human glioma. Real-time quantitative RT-PCR (qRT‑PCR), western blotting, and immunohistochemical staining were used to examine SPOP expression in glioma tissues and normal brain (NB) tissues. The relationships between the SPOP expression levels, the clinicopathological factors, and patient survival were investigated. The molecular mechanisms of SPOP expression and its effects on cell viability, migration and invasion were also explored by MTT assay, wound-healing assays and Transwell assay. SPOP mRNA and protein levels were downregulated in glioma tissues compared to NB. Immunohistochemical staining results showed low expression in 62.2% (61/98) of glioma samples, while high expression in 75% (9/12) of NB samples, and the difference was statistically significant (P=0.014). In addition, decreased SPOP was associated disease progression in glioma samples, the expression level of SPOP was positively correlated with mean tumor diameter (MTD) (P=0.021) and the status of tumor grade and histological type (WHO I, II, III and IV) (P=0.032) in glioma patients. Additionally, the overall survival of patients with low SPOP expression was significantly worse than that of SPOP-high patients (P=0.001). In vitro overexpression of SPOP markedly inhibited cell viability, migration and invasion in vitro. These findings suggest that SPOP has potential use as novel biomarker of glioma and may serve as an independent predictive factor for prognosis of glioma patients.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.3892/ijo.2014.2729 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
SPOP enhances FADD degradation and decreases the activeness of the NF-κB signaling pathway in prostate cancer: an study.
Transl Androl Urol
December 2024
Department of Urology, Xinjiang Medical University Affiliated Tumor Hospital, Urumqi, China.
Background: Speckle-type POZ protein (SPOP), FAS-associated protein with death domain (FADD), and nuclear transcription factor-κB (NF-κB) have been shown to be associated with the development of prostate cancer (PCa). FADD has been shown to activate the NF-κB pathway to promote tumorigenesis, while SPOP has been shown to enhance the breakdown of FADD and inhibit the function of the NF-κB signaling pathway in non-small cell lung cancer. The existence of this mechanism has not yet been confirmed in PCa.
View Article and Find Full Text PDFCul3 substrate adaptor SPOP targets Nup153 for degradation.
Mol Biol Cell
January 2025
Department of Chemistry and Biochemistry, University of California, Los Angeles, Los Angeles, CA 90095, USA.
SPOP is a Cul3 substrate adaptor responsible for the degradation of many proteins related to cell growth and proliferation. Because mutation or misregulation of SPOP drives cancer progression, understanding the suite of SPOP substrates is important to understanding the regulation of cell proliferation. Here, we identify Nup153, a component of the nuclear basket of the nuclear pore complex, as a novel substrate of SPOP.
View Article and Find Full Text PDFSpop deficiency impairs adipogenesis and promotes thermogenic capacity in mice.
PLoS Genet
December 2024
School of Biological Sciences, Anhui Province Key Laboratory of Translational Cancer Research, Bengbu Medical University, Bengbu, China.
As the adaptor protein that determines substrate specificity of the Cul3-SPOP-Rbx1 E3 ligase complex, SPOP is involved in numerous biological processes. However, its physiological connections with adipogenesis and thermogenesis remain poorly understood. In the current study, we report that the conditional knockout of Spop in mice results in substantial changes in protein expression, including the upregulation of a critical factor associated with thermogenesis, UCP1.
View Article and Find Full Text PDFCanonical androgen response element motifs are tumor suppressive regulatory elements in the prostate.
Nat Commun
December 2024
Department of Urology, Weill Cornell Medicine, New York, NY, USA.
The androgen receptor (AR) is central in prostate tissue identity and differentiation, and controls normal growth-suppressive, prostate-specific gene expression. It also drives prostate tumorigenesis when hijacked for oncogenic transcription. The execution of growth-suppressive AR transcriptional programs in prostate cancer (PCa) and the potential for reactivation remain unclear.
View Article and Find Full Text PDFTranscription and DNA replication collisions lead to large tandem duplications and expose targetable therapeutic vulnerabilities in cancer.
Nat Cancer
December 2024
Ben May Department for Cancer Research, University of Chicago, Chicago, IL, USA.
Despite the abundance of somatic structural variations (SVs) in cancer, the underlying molecular mechanisms of their formation remain unclear. In the present study, we used 6,193 whole-genome sequenced tumors to study the contributions of transcription and DNA replication collisions to genome instability. After deconvoluting robust SV signatures in three independent pan-cancer cohorts, we detected transcription-dependent, replicated-strand bias, the expected footprint of transcription-replication collision (TRC), in large tandem duplications (TDs).
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!