WNT‐5A, but not matrix metalloproteinase 3 or β‐catenin protein, expression is related to early stages of lip carcinogenesis

Xavier, Flávia Caló Aquino; Rodini, Camila Oliveira; Ramalho, Luciana Maria Pedreira; Mantesso, Andréa; Nunes, Fábio Daumas

doi:10.1111/j.1600-0714.2009.00756.x

Cited by 8 publications

(4 citation statements)

References 44 publications

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“…8 Upregulation of WNT5a appears conserved in squamous cell carcinomas from different anatomic locations, including the lip, head and neck, and lung, and appears to be an important gene in the tumorigenesis of squamous cell carcinoma. [56][57][58] Upregulation of WNT5a has been identified in many different malignancies, including melanoma and carcinomas from the breast, esophagus, lung, pancreas, and stomach. [59][60][61][62][63] MMP1 was found to be the most overexpressed gene in squamous cell carcinoma in comparison with normal skin (FC ¼ 48.51; Table 2).…”

Section: P53 Signalingmentioning

confidence: 99%

Molecular discrimination of cutaneous squamous cell carcinoma from actinic keratosis and normal skin

Hui

Binder

2011

Modern Pathology

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Actinic keratosis is widely believed to be a neoplastic lesion and a precursor to invasive squamous cell carcinoma. However, there has been some debate as to whether actinic keratosis is in fact actually squamous cell carcinoma and should be treated as such. As the clinical management and prognosis of patients is widely held to be different for each of these lesions, our goal was to identify unique gene signatures using DNA microarrays to discriminate among normal skin, actinic keratosis, and squamous cell carcinoma, and examine the molecular pathways of carcinogenesis involved in the progression from normal skin to squamous cell carcinoma. Formalin-fixed and paraffin-embedded blocks of skin: five normal skins (pooled), six actinic keratoses, and six squamous cell carcinomas were retrieved. The RNA was extracted and amplified. The labeled targets were hybridized to the Affymetrix human U133plus2.0 array and the acquisition and initial quantification of array images were performed using the GCOS (Affymetrix). The subsequent data analyses were performed using DNA-Chip Analyzer and Partek Genomic Suite 6.4. Significant differential gene expression (42 fold change, Po0.05) was seen with 382 differentially expressed genes between squamous cell carcinoma and normal skin, 423 differentially expressed genes between actinic keratosis and normal skin, and 9 differentially expressed genes between actinic keratosis and squamous cell carcinoma. The differentially expressed genes offer the possibility of using DNA microarrays as a molecular diagnostic tool to distinguish between normal skin, actinic keratosis, and squamous cell carcinoma. In addition, the differentially expressed genes and their molecular pathways could be potentially used as prognostic markers or targets for future therapeutic innovations.

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Section: P53 Signalingmentioning

confidence: 99%

Molecular discrimination of cutaneous squamous cell carcinoma from actinic keratosis and normal skin

Hui

Binder

2011

Modern Pathology

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“…The upregulation of MMP3 was validated and identified as a signature in oral squamous cell carcinoma progression (37). Immunohistochemistry revealed the involvement of MMP3 in the events correlated with lip SCC (38). Although not validated, MMP3 was found to be upregulated in LSCC and associated with the development of invasion (39).…”

Section: Discussionmentioning

confidence: 99%

Identification of biomarkers with a tumor stage-dependent expression and exploration of the mechanism involved in laryngeal squamous cell carcinoma

Hui

Yang

et al. 2015

Oncology Reports

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The aim of this study was to identify biomarkers with a tumor stage-dependent expression manner and explore the regulatory mechanisms of laryngeal squamous cell carcinoma (LSCC) progression. Microarray data GSE59102 was used for differential analysis using a limma package. Enrichment analyses were performed for the differentially expressed genes (DEGs) between tumor tissues and normal tissues at different stages. A co-expressed network involving the overlapped DEGs in two stages was established based on Pearson's correlation coefficients. Furthermore, for the tumor stage‑dependent expressed DEGs, a protein‑protein interaction (PPI) network was constructed by mapping the genes using the STRING database. Transcription factors (TFs), oncogenes and tumor‑associated genes (TSGs) among the DEGs were predicted, following a search of the TRANSFAC, tumor-associated gene (TAG) and TSG databases. The CDT database was used to identify LSCC‑associated genes. In total, 696 DEGs from early stage and control samples and 622 DEGs from advanced sttage and control samples were selected, which were mainly enriched in the cell cycle pathway. In the co-expressed network, BUB1, TTK, E2F1 and CEP55 were prominent, with E2F1 being predicted as a TSG and CEP55 as an oncogene. The HOX family members were predicted as TFs. MMP1, MMP9, MMP3 and PLAU were the most evident nodes in the PPI network, where MMP3 was connected with MMP1. The ADH family was correlated with LSCC. Several biomarkers with tumor stage-dependent expression were identified including MMP1, MMP3, MMP9, PLAU and ADHs. Additionally, the dysregulated cell cycle pathway involving BUB1, TTK, E2F1 and CEP55, and the mediation of MMP1 by MMP3 as well as the predicted TF HOX, may all play significant roles in LSCC progression.

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“…These results are contrary to our expectations at the time of planning this study; we expected that Wnt protein would show more prominent IHC staining in IP with dysplasia or IP with SCC. Wnt-1 was selected as a candidate marker based on a study performed in 2008 by Xavier et al , 17 who reported that Wnt protein was not expressed in normal epithelium but was highly expressed in early-stage lip cancer. However, another study presented contradictory findings, that Wnt-1 was concurrently expressed in normal tissue and cancer tissue of colorectal epithelium and that normal epithelium showed stronger staining than cancer tissue.…”

Section: Discussionmentioning

confidence: 99%

“…16 In the canonical pathway, Wnt signaling plays a key role in signal transduction, and without Wnt signaling intracellular ␤-catenin is proteolytically degraded by a protein complex. 17 However, in the presence of Wnt signaling, the function of the degradation complex is inhibited and the intracellular level of ␤-catenin increases, which results in intracellular accumulation and nuclear translocation of ␤-catenin. 18 Translocated ␤-catenin can initiate transcription of several target genes, e.g., cyclin D1, which results in progression toward malignancy.…”

mentioning

confidence: 99%

Role of Wnt Signaling Pathway in Progression of Sinonasal Inverted Papilloma to Squamous Cell Carcinoma

Jung

Lee

Kim

et al. 2015

Am J Rhinol�Allergy

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WNT‐5A, but not matrix metalloproteinase 3 or β‐catenin protein, expression is related to early stages of lip carcinogenesis

Cited by 8 publications

References 44 publications

Molecular discrimination of cutaneous squamous cell carcinoma from actinic keratosis and normal skin

Molecular discrimination of cutaneous squamous cell carcinoma from actinic keratosis and normal skin

Identification of biomarkers with a tumor stage-dependent expression and exploration of the mechanism involved in laryngeal squamous cell carcinoma

Role of Wnt Signaling Pathway in Progression of Sinonasal Inverted Papilloma to Squamous Cell Carcinoma

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