Overexpression of a set of genes, including WISP-1, common to pulmonary metastases of both mouse D122 Lewis lung carcinoma and B16-F10.9 melanoma cell lines

Margalit, Ofer; Eisenbach, Lea; Amariglio, Ninette; Kaminski, Naftali; Harmelin, Alon; Pfeffer, Raphael; Shohat, M; Rechavi, Gideon; Berger, Raanan

doi:10.1038/sj.bjc.6600977

Cited by 37 publications

(28 citation statements)

References 29 publications

(30 reference statements)

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“…31 It was also essential for the metastatic process and specifically for pulmonary metastases. 32 For RAMP1, its expression was increased in cancer cells, 33 and the role of RAMP1 was reported to be a promotor in prostate tumorigenesis and as a novel biomarker, and possible therapeutic target in prostate cancer. 34 Thus, WISP1 and RAMP1 could be the potential candidates of biopsy indexes and potential therapy targets of lung adenocarcinoma.…”

Section: Discussionmentioning

confidence: 98%

Abnormal gene expression and gene fusion in lung adenocarcinoma with high-throughput RNA sequencing

et al. 2014

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To explore the universal law of the abnormal gene expression and the structural variation of genes related to lung adenocarcinoma, the gene expression profile of GSE37765 were downloaded from Gene Expression Omnibus database. The differentially expressed genes (DEGs) were analyzed with t-test and NOISeq tool, and the core DEGs were screened out by combining with another RNA-seq data containing totally 77 pairs of samples in 77 patients with lung adenocarcinoma. Moreover, the functional annotation of the core DEGs was performed by using the Database for Annotation Visualization and Integrated Discovery following selection of oncogene and tumor suppressor by combining with tumor suppressor genes and Cancer Genes database, and motif-finding of core DEGs was performed with motif-finding algorithm Seqpos. We also used Tophat-fusion tool to further explore the fusion genes. In total, 850 downregulated DEGs and 206 upregulated DEGs were screened out in lung adenocarcinoma tissues. Next, we selected 543 core DEGs, including 401 downregulated and 142 upregulated genes, and vasculature development (P=1.89E-06) was significantly enriched among downregulated core genes, as well as mitosis (P=6.26E-04) enriched among upregulated core genes. On the basis of the cellular localization analysis of core genes, wnt-1-induced secreted protein 1 (WISP1) and receptor (G protein-coupled) activity modifying protein 1 (RAMP1) identified mainly located in extracellular region and extracellular space. We also screened one oncogene, v-myb avian myeloblastosis viral oncogene homolog-like 2 (MYBL2). Moreover, transcription factor GATA2 was mined by motif-finding analysis. Finally, four fusion genes belonged to the human leukocyte antigen (HLA) family. WISP1, RAMP1, MYBL2 and GATA2 could be potential targets of treatment for lung adenocarcinoma and the fusion of HLA family genes might have important roles in lung adenocarcinoma.

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Section: Discussionmentioning

confidence: 98%

Abnormal gene expression and gene fusion in lung adenocarcinoma with high-throughput RNA sequencing

et al. 2014

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“…Notably, increased WISP-1 expression has been identified in several cancer types, including colorectal cancer, hepatocellular carcinoma, lung carcinoma, breast, esophageal and endometrial cancer (5)(6)(7)(8)10,(13)(14)(15). Furthermore, WISP-1 expression has also been revealed to be low in healthy lung epithelial cells, but significantly upregulated in lung cancer tissue (15).…”

Section: Discussionmentioning

confidence: 99%

“…The ECM modulates cellular responses, including cell growth, differentiation and survival (2)(3)(4). Since the first identification of human WISP-1 in an epithelial cell line in 1998, WISP-1 expression has been studied in various organs and disease states, including malignant diseases, such as colorectal cancer, hepatocellular carcinoma, lung carcinoma and breast cancer, and nonmalignant diseases, including lung fibrosis (5)(6)(7)(8)(9)(10). WISP-1 is strongly expressed in primary breast cancer and rectal cancer, and increased WISP-1 expression is associated with more aggressive features of cancer progression (8,10).…”

Section: Introductionmentioning

confidence: 99%

WNT1-inducible signaling pathway protein-1 contributes to tumor progression and treatment failure in oral squamous cell carcinoma

et al. 2017

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Abstract. WNT1-inducible-signaling pathway protein-1 (WISP-1) belongs to the family of cysteine rich 61/connective tissue growth factor/nephroblastoma overexpressed matricellular proteins, which are involved in various biological processes, including cell adhesion, proliferation, differentiation, angiogenesis and carcinogenesis. In the present study, the expression of WISP-1 was investigated, and its association with clinicopathological factors and prognosis in patients with oral squamous cell carcinoma (OSCC) was evaluated. Additionally, the role of WISP-1 in invasion and apoptosis of human OSCC cells was evaluated. Immunoreactivity of WISP-1 was increased in OSCC tissue compared with adjacent normal tissue samples. High expression of WISP-1 protein was observed in 24/84 (28.57%) OSCC specimens. Additionally, high WISP-1 expression was significantly associated with treatment failure (P=0.042). The 5-year overall survival rate was 33% in patients with high WISP1 expression, and 66% in patients with low WISP-1 expression. WISP-1 expression in the human OSCC SCC-1483 cell line was observed. Furthermore, WISP-1 knockdown using small interfering (si)RNA significantly reduced cell invasion and induced apoptosis compared with control siRNA-transfected cells. These findings suggested that WISP-1 is associated with tumor progression and poor prognosis by increasing tumor cell invasion and inhibiting cell apoptosis in human OSCC.

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“…1). Indeed, WISP1 alterations have been reported in lung cancer specimens [61,62,63]. In addition, increased activity of the upstream WNT/β-catenin pathway has also been reported.…”

Section: Oncogenic Signaling Pathwaysmentioning

confidence: 98%

Lung Cancer in Pulmonary Fibrosis: Tales of Epithelial Cell Plasticity

Königshoff

2011

Respiration

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Lung epithelial cells exhibit a high degree of plasticity. Alterations to lung epithelial cell function are critically involved in several chronic lung diseases such as pulmonary fibrosis. Pulmonary fibrosis is characterized by repetitive injury and subsequent impaired repair of epithelial cells, which leads to aberrant growth factor activation and fibroblast accumulation. Increased proliferation and hyper- and metaplasia of epithelial cells upon injury have also been observed in pulmonary fibrosis; this epithelial cell activation might represent the basis for lung cancer development. Indeed, several studies have provided histopathological evidence of an increased incidence of lung cancer in pulmonary fibrosis. The mechanisms involved in the development of cancer in pulmonary fibrosis, however, remain poorly understood. This review highlights recently uncovered molecular mechanisms shared between lung cancer and fibrosis, which extend the current evidence of a common trait of cancer and fibrosis, as provided by histopathological observations.

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Overexpression of a set of genes, including WISP-1, common to pulmonary metastases of both mouse D122 Lewis lung carcinoma and B16-F10.9 melanoma cell lines

Cited by 37 publications

References 29 publications

Abnormal gene expression and gene fusion in lung adenocarcinoma with high-throughput RNA sequencing

Abnormal gene expression and gene fusion in lung adenocarcinoma with high-throughput RNA sequencing

WNT1-inducible signaling pathway protein-1 contributes to tumor progression and treatment failure in oral squamous cell carcinoma

Lung Cancer in Pulmonary Fibrosis: Tales of Epithelial Cell Plasticity

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