Increased expression of CELSR3 indicates a poor prognostic factor for Prostate Cancer

Chen, Xuanrong; Ma, Qianwang; Liu, Yixi; Han-ling, LI; Liu, Zihao; Zhang, Zheng; Niu, Yuanjie; Shang, Zhiqun

doi:10.7150/jca.49567

Cited by 15 publications

(8 citation statements)

References 27 publications

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“…Cell growth was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphe-nyltetrazolium bromide proliferation assays. Migration assay was performed using Transwell chambers of 8μm pore size (Corning) as described before [ 37 ].…”

Section: Methodsmentioning

confidence: 99%

Androgen deprivation restores ARHGEF2 to promote neuroendocrine differentiation of prostate cancer

et al. 2022

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Androgen receptor (AR) plays an important role in the progression of prostate cancer and has been targeted by castration or AR-antagonists. The emergence of castration-resistant prostate cancer (CRPC) after androgen deprivation therapy (ADT) is inevitable. However, it is not entirely clear how ADT fails or how it causes resistance. Through analysis of RNA-seq data, we nominate ARHGEF2 as a pivotal androgen-repressed gene. We show that ARHGEF2 is directly suppressed by androgen/AR. AR occupies the enhancer and communicates with the promoter region of ARHGEF2. Functionally, ARHGEF2 is important for the growth, lethal phenotype, and survival of CRPC cells and tumor xenografts. Correspondingly, AR inhibition or AR antagonist treatment can restore ARHGEF2 expression, thereby allowing prostate cancer cells to induce treatment resistance and tolerance. Overall, our findings provide an explanation for the contradictory clinical results that ADT resistance may be caused by the up-regulation of ARHGEF2 and provide a novel target.

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Section: Methodsmentioning

confidence: 99%

Androgen deprivation restores ARHGEF2 to promote neuroendocrine differentiation of prostate cancer

et al. 2022

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“…It might also participate in the Paris forrestii antitumor effect [ 9 ]. Besides, CELSR3 downregulation significantly suppresses PRAD cell proliferation and migration [ 10 ]. MSH5 has been reported as a pleiotropic susceptibility locus for several cancers and was identified as a novel candidate gene warranting additional follow-up as a prospective PRAD risk locus [ 11 ].…”

Section: Resultsmentioning

confidence: 99%

Tumor-antigens and immune landscapes identification for prostate adenocarcinoma mRNA vaccine

Zheng

et al. 2021

Mol Cancer

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Prostate adenocarcinoma (PRAD) is a leading cause of death among men. Messenger ribonucleic acid (mRNA) vaccine presents an attractive approach to achieve satisfactory outcomes; however, tumor antigen screening and vaccination candidates show a bottleneck in this field. We aimed to investigate the tumor antigens for mRNA vaccine development and immune subtypes for choosing appropriate patients for vaccination. We identified eight overexpressed and mutated tumor antigens with poor prognostic value of PRAD, including KLHL17, CPT1B, IQGAP3, LIME1, YJEFN3, KIAA1529, MSH5 and CELSR3. The correlation of those genes with antigen-presenting immune cells were assessed. We further identified three immune subtypes of PRAD (PRAD immune subtype [PIS] 1–3) with distinct clinical, molecular, and cellular characteristics. PIS1 showed better survival and immune cell infiltration, nevertheless, PIS2 and PIS3 showed cold tumor features with poorer prognosis and higher tumor genomic instability. Moreover, these immune subtypes presented distinguished association with immune checkpoints, immunogenic cell death modulators, and prognostic factors of PRAD. Furthermore, immune landscape characterization unraveled the immune heterogeneity among patients with PRAD. To summarize, our study suggests KLHL17, CPT1B, IQGAP3, LIME1, YJEFN3, KIAA1529, MSH5 and CELSR3 are potential antigens for PRAD mRNA vaccine development, and patients in the PIS2 and PIS3 groups are more suitable for vaccination.

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“…Low expression of CELSR3 significantly reduces the migration and invasion of lung adenocarcinoma cells ( Li et al, 2021 ). CELSR3 expression may serve as a prognostic biomarker in patients with prostate cancer and may predict poor outcomes ( Chen et al, 2021 ). In addition, CELSR3 is highly expressed in liver and oral cancers and associated with a poor prognosis ( Gu et al, 2019 ; Zheng et al, 2022 ).…”

Section: Discussionmentioning

confidence: 99%

Identification and validation of a novel tumor driver gene signature for diagnosis and prognosis of head and neck squamous cell carcinoma

Liu

Liu²,

Ding³

et al. 2022

Front. Mol. Biosci.

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Objective: Head and neck squamous cell carcinoma (HNSCC) is a common heterogeneous cancer with complex carcinogenic factors. However, the current TNM staging criteria to judge its severity to formulate treatment plans and evaluate the prognosis are particularly weak. Therefore, a robust diagnostic model capable of accurately diagnosing and predicting HNSCC should be established.Methods: Gene expression and clinical data were retrieved from The Cancer Genome Atlas and Gene Expression Omnibus databases. Key prognostic genes associated with HNSCC were screened with the weighted gene co-expression network analysis and least absolute shrinkage and selection operator (LASSO) Cox regression model analysis. We used the timeROC and survival R packages to conduct time-dependent receiver operating characteristic curve analyses and calculated the area under the curve at different time points of model prediction. Patients in the training and validation groups were divided into high- and low-risk subgroups, and Kaplan-Meier (K-M) survival curves were plotted for all subgroups. Subsequently, LASSO and support vector machine algorithms were used to screen genes to construct diagnostic model. Furthermore, we used the Wilcoxon signed-rank test to compare the half-maximal inhibitory concentrations of common chemotherapy drugs among patients in different risk groups. Finally, the expression levels of eight genes were measured using quantitative real-time polymerase chain reaction and immunohistochemistry.Results: Ten genes (SSB, PFKP, NAT10, PCDH9, SHANK2, PAX8, CELSR3, DCLRE1C, MAP2K7, and ODF4) with prognostic potential were identified, and a risk score was derived accordingly. Patients were divided into high- and low-risk groups based on the median risk score. The K-M survival curves confirmed that patients with high scores had significantly worse overall survival. Receiver operating characteristic curves proved that the prognostic signature had good sensitivity and specificity for predicting the prognosis of patients with HNSCC. Univariate and multivariate Cox regression analyses confirmed that the gene signature was an independent prognostic risk factor for HNSCC. Diagnostic model was built by identifying eight genes (SSB, PFKP, NAT10, PCDH9, CELSR3, DCLRE1C, MAP2K7, and ODF4). The high-risk group showed higher sensitivity to various common chemotherapeutic drugs. DCLRE1C expression was higher in normal tissues than in HNSCC tissues.Conclusion: Our study identified the important role of tumor-driver genes in HNSCC and their potential clinical diagnostic and prognostic values to facilitate individualized management of patients with HNSCC.

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Increased expression of CELSR3 indicates a poor prognostic factor for Prostate Cancer

Cited by 15 publications

References 27 publications

Androgen deprivation restores ARHGEF2 to promote neuroendocrine differentiation of prostate cancer

Androgen deprivation restores ARHGEF2 to promote neuroendocrine differentiation of prostate cancer

Tumor-antigens and immune landscapes identification for prostate adenocarcinoma mRNA vaccine

Identification and validation of a novel tumor driver gene signature for diagnosis and prognosis of head and neck squamous cell carcinoma

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