Gene Expression Profiling of Prostate Cancer–Associated Genes Identifies Fibromodulin as Potential Novel Biomarker for Prostate Cancer

Bettin, Alfonso; Reyes, Ismael; Reyes, Niradiz

doi:10.5301/jbm.5000184

Cited by 33 publications

(28 citation statements)

References 47 publications

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“…; Bettin et al . ). The goal of this study was to investigate the expression pattern of this gene in prostate cancer tissue and across different prostate lesions, namely PIA and HGPIN.…”

Section: Discussionmentioning

confidence: 97%

“…) and human origin (Bettin et al . ). CXXC5, also referred to as retinoid‐inducible nuclear factor (RINF), is a gene localized to the 5q31.3 chromosomal region, which encodes a retinoid‐inducible nuclear protein containing a CXXC‐type zinc finger motif (Pendino et al .…”

mentioning

confidence: 97%

“…The identification of genes specifically deregulated in this neoplasia may uncover new oncogenes or tumour suppressors with clinical relevance for diagnosis, prognosis and/or therapy. We have previously reported the differential expression of CXXC5 in metastatic prostate cancer cell lines of both rat (Reyes et al 2007) and human origin (Bettin et al 2016). CXXC5, also referred to as retinoid-inducible nuclear factor (RINF), is a gene localized to the 5q31.3 chromosomal region, which encodes a retinoid-inducible nuclear protein containing a CXXC-type zinc finger motif (Pendino et al 2009).…”

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confidence: 99%

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CXXC5 expression in prostate cancer: implications for cancer progression

Benedetti

Marzo

Geliebter

et al. 2017

Int J Experimental Path

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Identification of genes specifically deregulated in prostate adenocarcinoma may lead to discovery of new oncogenes/tumour suppressors with clinical relevance for diagnosis, prognosis and/or therapy. CXXC5 is a gene encoding a retinoid-inducible nuclear factor, whose overexpression in breast tumours, metastatic malignant melanomas and papillary thyroid carcinoma has been recently reported. We previously found differential expression of CXXC5 transcripts in metastatic prostate cancer cell lines of both rat and human origin. However, knowledge on the expression of this gene in benign or malignant human prostate tissue is lacking. The aim of this study was to determine the mRNA and protein expression pattern of CXXC5 in human benign prostate tissue, proliferative inflammatory atrophy, high-grade prostatic intra-epithelial neoplasia and prostate cancer, using qPCR, chromogenic in situ hybridization and immunohistochemistry. Our results showed that protein levels determined by immunohistochemistry were in agreement with transcript levels observed by chromogenic in situ hybridization. CXXC5 mRNA and protein expressions were significantly higher in prostate cancer, high-grade prostatic intra-epithelial neoplasia, and proliferative inflammatory atrophy, compared to benign prostate tissue. Significantly, within the same tissue specimens, CXXC5 staining was stronger in malignant acini than in matched adjacent, benign acini; immunostaining for this protein was mainly localized to the nucleus of benign epithelial cells and both the nucleus and cytoplasm of malignant epithelial cells. Our findings suggest that CXXC5 may play a role in the process of prostate carcinogenesis. Additional studies are required to determine the biological and clinical significance of CXXC5 in prostate cancer development and/or progression.

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“…; Bettin et al . ). The goal of this study was to investigate the expression pattern of this gene in prostate cancer tissue and across different prostate lesions, namely PIA and HGPIN.…”

Section: Discussionmentioning

confidence: 97%

mentioning

confidence: 97%

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confidence: 99%

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CXXC5 expression in prostate cancer: implications for cancer progression

Benedetti

Marzo

Geliebter

et al. 2017

Int J Experimental Path

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“…Screening of individuals without any cardinal symptom by the PSA test has been the focus of increasing criticism, primarily due to potential overtreatment and less comprehensive evaluation [45]. Candidate biomarkers will be separated with groups as molecular class, soluble proteins DNA methylation, mRNA, microRNA, and so forth [46–48].…”

Section: Epigenetic Biomarkers In Prostate Cancermentioning

confidence: 99%

“…SOX2 was consistently downregulated, except in cell clusters lying within lymph node- (LN-) positive prostate cancer [58]. Some other special genes could be found to predict recurrence as XPO6 [59] and FMOD as biomarker for prostate cancer [45]. …”

Section: Epigenetic Biomarkers In Prostate Cancermentioning

confidence: 99%

New Progress of Epigenetic Biomarkers in Urological Cancer

Cao

2016

Disease Markers

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Urological cancers consist of bladder, kidney, prostate, and testis cancers and they are generally silenced at their early stage, which leads to the loss of the best opportunity for early diagnosis and treatment. Desired biomarkers are scarce for urological cancers and current biomarkers are lack of specificity and sensitivity. Epigenetic alterations are characteristic of nearly all kinds of human malignances including DNA methylation, histone modification, and miRNA regulation. Besides, the detection of these epigenetic conditions is easily accessible especially for urine, best target for monitoring the diseases of urinary system. Here, we summarize some new progress about epigenetic biomarkers in urological cancers, hoping to provide new thoughts for the diagnosis, treatment, and prognosis of urological cancers.

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Downregulation of fibromodulin attenuates inflammatory signaling and atrial fibrosis in spontaneously hypertensive rats with atrial fibrillation via inhibiting TLR4/NLRP3 signaling pathway

Liang,

Zhou,

Wang

et al. 2023

Immunity Inflam & Disease

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BackgroundMyocardial fibrosis is an important factor in the induction and maintenance of atrial fibrillation (AF). Fibromodulin (FMOD) promotes fibrotic gene expression. However, its specific role in spontaneously hypertensive rats (SHR)‐AF remains unclear.MethodsWe analyzed FMOD mRNA and protein expression in rat atrial tissues using RT‐qPCR, Western blot analysis, and immunohistochemistry. Histopathological examination of atrial tissues was performed using hematoxylin and eosin (H&E), Masson's trichrome, and Picrosirius red staining. The levels of inflammatory and fibrosis‐related proteins were measured using Western blot analysis.ResultsFMOD relative mRNA and protein expression levels were notably upregulated in atrial tissues of both AF groups (normal‐AF and SHR‐AF groups) than that in atrial tissues of the no‐AF group (normal and SHR group). This effect was particularly pronounced in the SHR‐AF group. Pathological changes revealed that the extracellular matrix, collagen, collagen fibers, and left atrial diameter were notably increased in the atrial tissues from the SHR‐AF group compared to those in the atrial tissues from the SHR group, whereas the left ventricular fractional shortening and left ventricular ejection fraction were notably lower. Expression of TLR4, MyD88, NLRP3, TGF‐β1, collagen I, and collagen II mRNA were clearly higher in atrial tissues from the SHR‐AF group than in those from the SHR group. Protein levels of TLR4, MyD88, NLRP3, Cleavage‐Caspase‐1, Cleavage‐IL‐1β, TGF‐β1, p‐Smad2, collagen I, and collagen II were clearly higher in atrial tissues from the SHR‐AF group than in those from the SHR group. FMOD knockdown inhibited atrial fibrosis, collagen accumulation, and the TLR4/MyD88/NLRP3 signaling pathway.ConclusionDownregulation of FMOD attenuated inflammatory signaling and atrial fibrosis in SHR‐AF by inhibiting the TLR4/NLRP3 signaling pathway. Therefore, FMOD may be a promising therapeutic target in AF.

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Gene Expression Profiling of Prostate Cancer–Associated Genes Identifies Fibromodulin as Potential Novel Biomarker for Prostate Cancer

Cited by 33 publications

References 47 publications

CXXC5 expression in prostate cancer: implications for cancer progression

CXXC5 expression in prostate cancer: implications for cancer progression

New Progress of Epigenetic Biomarkers in Urological Cancer

Downregulation of fibromodulin attenuates inflammatory signaling and atrial fibrosis in spontaneously hypertensive rats with atrial fibrillation via inhibiting TLR4/NLRP3 signaling pathway

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