Expression profiles and prognostic significance of WNT family members in glioma via bioinformatic analysis

Xu, Anqi; Yang, Huiping; Gao, Kunjie; Zhan, Zhengming; Song, Zibin; Huang, Tengyue; Song, Ye

doi:10.1042/bsr20194255

Cited by 16 publications

(11 citation statements)

References 57 publications

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“…The expression of WNT5B has been shown in gliomas and atypical teratoid rhabdoid tumors (ATRT), but studies beyond gene expression have not been performed. WNT5B expression was correlated with better overall survival, in contrast to patients with elevated WNT5A expression that had overall worse survival ( Xu et al, 2020 ). In a set of ATRT samples, WNT5B was upregulated in 19 of the 20 samples.…”

Section: Role Of Wnt5b In Cancermentioning

confidence: 99%

WNT5B in Physiology and Disease

Suthon

Perkins

Bryja

et al. 2021

Front. Cell Dev. Biol.

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WNT5B, a member of the WNT family of proteins that is closely related to WNT5A, is required for cell migration, cell proliferation, or cell differentiation in many cell types. WNT5B signals through the non-canonical β-catenin-independent signaling pathway and often functions as an antagonist of canonical WNT signaling. Although WNT5B has a high amino acid identity with WNT5A and is often assumed to have similar activities, WNT5B often exhibits unique expression patterns and functions. Here, we describe the distinct effects and mechanisms of WNT5B on development, bone, adipose tissue, cardiac tissue, the nervous system, the mammary gland, the lung and hematopoietic cells, compared to WNT5A. We also highlight aberrances in non-canonical WNT5B signaling contributing to diseases such as osteoarthritis, osteoporosis, obesity, type 2 diabetes mellitus, neuropathology, and chronic diseases associated with aging, as well as various cancers.

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Section: Role Of Wnt5b In Cancermentioning

confidence: 99%

WNT5B in Physiology and Disease

Suthon

Perkins

Bryja

et al. 2021

Front. Cell Dev. Biol.

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“…We found that in females but not males p53 R172H localization is enriched at AP-2gamma DNA-binding motifs. WNT5A has been shown to be upregulated in glioma and is associated with poor overall survival 52 . In our model, Wnt5a mRNA was significantly upregulated in female p53 R172H and down regulated in male p53 R172H .…”

Section: Resultsmentioning

confidence: 99%

p53 mutations exhibit sex specific gain-of-function activity in gliomagenesis

Rockwell

Yang

Warrington

et al. 2021

Preprint

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The tumor suppressor TP53 is the most frequently mutated gene in cancer. Most TP53 mutations are missense mutations in the DNA-binding domain, which in addition to loss of canonical p53 activity, frequently confer gain-of-function (GOF) aberrant transcriptional activity through mutant p53 localization to non-canonical genes. GOF phenotypes differ by mutation and cell identity and are reported to include increased proliferation, migration, metabolic reprogramming, and therapy resistance. We found that several recurring p53 mutations exhibit a sex-bias in patients with glioblastoma (GBM). In vitro and in vivo analysis of three mutations, p53R172H, p53Y202C, and p53Y217C revealed sex differences in each mutation′s ability to transform primary mouse astrocytes. p53R172H exhibited a far greater ability to transform female astrocytes than males, p53Y202C transformed both male and female astrocytes with a small male bias, and p53Y217C only exhibited GOF transformation effects in male astrocytes. These phenotypic differences reflect an interaction between sex and GOF mutation to drive unique gene expression patterns in cancer pathways. We found that mutant p53 exhibits sex and mutation specific aberrant genomic localization to the transcriptional start sites of upregulated genes, whose promoter regions were enriched for different sets of transcription factor DNA-binding motifs. Together, our data establish a novel paradigm for sex specific mutant p53 GOF activity in GBM with implications for all cancer.

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“…We evidenced that a very large number of genes involved in gains and shared between TCs and GSCs belong to the GO term cellular component, particularly extracellular space, extracellular region and membrane, indicating a strong involvement in intercellular signaling. Interestingly, several gained genes shared between at least two datasets were reported in the literature as overexpressed in high-grade gliomas, associated with poor prognosis, or in any case, involved in canonical pathways of GBM ( EIF2AK1 , FTL , SRC , GNG8 , GNG11 , GNG7 , FZD9 , GNB2 , TGM2 ) [ 45 , 46 , 47 , 48 , 49 ]. Conversely, only one lost gene, AKR1C2 , shared between at least two datasets, was reported as downregulated and associated with high-risk-score glioma in the REMBRANDT data set [ 50 ].…”

Section: Discussionmentioning

confidence: 99%

Characterizing the Genomic Profile in High-Grade Gliomas: From Tumor Core to Peritumoral Brain Zone, Passing through Glioma-Derived Tumorspheres

Giambra

Messuti

Cristofori

et al. 2021

Biology

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Glioblastoma is an extremely heterogeneous disease. Treatment failure and tumor recurrence primarily reflect the presence in the tumor core (TC) of the glioma stem cells (GSCs), and secondly the contribution, still to be defined, of the peritumoral brain zone (PBZ). Using the array-CGH platform, we deepened the genomic knowledge about the different components of GBM and we identified new specific biomarkers useful for new therapies. We firstly investigated the genomic profile of 20 TCs of GBM; then, for 14 cases and 7 cases, respectively, we compared these genomic profiles with those of the related GSC cultures and PBZ biopsies. The analysis on 20 TCs confirmed the intertumoral heterogeneity and a high percentage of copy number alterations (CNAs) in GBM canonical pathways. Comparing the genomic profiles of 14 TC-GSC pairs, we evidenced a robust similarity among the two samples of each patient. The shared imbalanced genes are related to the development and progression of cancer and in metabolic pathways, as shown by bioinformatic analysis using DAVID. Finally, the comparison between 7 TC-PBZ pairs leads to the identification of PBZ-unique alterations that require further investigation.

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Expression profiles and prognostic significance of WNT family members in glioma via bioinformatic analysis

Cited by 16 publications

References 57 publications

WNT5B in Physiology and Disease

WNT5B in Physiology and Disease

p53 mutations exhibit sex specific gain-of-function activity in gliomagenesis

Characterizing the Genomic Profile in High-Grade Gliomas: From Tumor Core to Peritumoral Brain Zone, Passing through Glioma-Derived Tumorspheres

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