BNF-1, a novel gene encoding a putative extracellular matrix protein, is overexpressed in tumor tissues

Wu, Inmin; Moses, Marsha A.

doi:10.1016/s0378-1119(03)00563-8

Cited by 19 publications

(20 citation statements)

References 13 publications

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“…Moreover, CHRDL2 levels correlated with clinical features, such as tumor size, TNM staging, and tumor differentiation, and all of these parameters were independent factors for CRC survival. This is consistent with previous observations that CHRDL2 expression was increased in breast, lung and colon cancers, suggesting that CHRDL2 promotes tumorigenesis [21]. Our survival rate and Cox proportional hazards model analyses showed that high CHRDL2 expression levels correlate with poor prognosis in CRC.…”

Section: Discussionsupporting

confidence: 93%

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Overexpression of colorectal cancer oncogene CHRDL2 predicts a poor prognosis

et al. 2016

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Bone morphogenetic proteins (BMPs) both promote and suppress tumorigenesis, and multiple BMP antagonists reportedly contribute to cancer progression. In this study, we demonstrated that the BMP antagonist Chordin-like 2 (CHRDL2) is upregulated in colorectal cancer (CRC) tissues, and that CHRDL2 levels correlate with clinical features of CRC patients, including tumor size, TNM staging, and tumor differentiation. In addition, survival rate and Cox proportional hazards model analyses showed that high CHRDL2 levels correlate with a poor prognosis in CRC. Moreover, CHRDL2 promoted CRC cell proliferation in vitro and in vivo, perhaps through up-regulation of Cyclin D1 and down-regulation of P21. Co-immunoprecipitation assays showed that CHRDL2 bound to BMPs, which inhibited p-Smad1/5, thereby promoting CRC cell proliferation and inhibiting apoptosis. These results suggest CHRDL2 could serve as a biomarker of poor prognosis in CRC, and provide evidence that CHRDL2 acts as an oncogene in human CRC, making it a novel potential therapeutic target.

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Section: Discussionsupporting

confidence: 93%

“…Although a previous study showed higher levels of CHRDL2 mRNA in breast cancer [21], CHRDL2's role in tumorigenesis remains largely unknown. Here, we measured CHRDL2 levels in human CRC tissue to investigate potential correlations between CHRDL2 expression and CRC clinicopathologic features as well as patient prognosis.…”

Section: Introductionmentioning

confidence: 99%

Overexpression of colorectal cancer oncogene CHRDL2 predicts a poor prognosis

et al. 2016

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“…CHRDL2 encodes a putative extracellular matrix protein and was shown to be over-expressed in breast, lung and colon tumors, compared with corresponding normal tissues (59). REC8 , located at 14q12, is part of the cohesin gene family.…”

Section: Discussionmentioning

confidence: 99%

Recurrent genomic alterations in sequential progressive leukoplakia and oral cancer: drivers of oral tumorigenesis?

Cervigne

Machado²,

Goswami

et al. 2014

Human Molecular Genetics

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A significant proportion (up to 62%) of oral squamous cell carcinomas (OSCCs) may arise from oral potential malignant lesions (OPMLs), such as leukoplakia. Patient outcomes may thus be improved through detection of lesions at a risk for malignant transformation, by identifying and categorizing genetic changes in sequential, progressive OPMLs. We conducted array comparative genomic hybridization analysis of 25 sequential, progressive OPMLs and same-site OSCCs from five patients. Recurrent DNA copy number gains were identified on 1p in 20/25 cases (80%) with minimal, high-level amplification regions on 1p35 and 1p36. Other regions of gains were frequently observed: 11q13.4 (68%), 9q34.13 (64%), 21q22.3 (60%), 6p21 and 6q25 (56%) and 10q24, 19q13.2, 22q12, 5q31.2, 7p13, 10q24 and 14q22 (48%). DNA losses were observed in >20% of samples and mainly detected on 5q31.2 (35%), 16p13.2 (30%), 9q33.1 and 9q33.29 (25%) and 17q11.2, 3p26.2, 18q21.1, 4q34.1 and 8p23.2 (20%). Such copy number alterations (CNAs) were mapped in all grades of dysplasia that progressed, and their corresponding OSCCs, in 70% of patients, indicating that these CNAs may be associated with disease progression. Amplified genes mapping within recurrent CNAs (KHDRBS1, PARP1, RAB1A, HBEGF, PAIP2, BTBD7) were selected for validation, by quantitative real-time PCR, in an independent set of 32 progressive leukoplakia, 32 OSSCs and 21 non-progressive leukoplakia samples. Amplification of BTBD7, KHDRBS1, PARP1 and RAB1A was exclusively detected in progressive leukoplakia and corresponding OSCC. BTBD7, KHDRBS1, PARP1 and RAB1A may be associated with OSCC progression. Protein–protein interaction networks were created to identify possible pathways associated with OSCC progression.

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“…29 Another extracellular matrix component, CHRDL2, also known as BNF-1, is found to be upregulated in tumors. 30 Disintegrin and metalloproteinases ADAMS and ADAMTS are involved in various biological events and many of them are expressed in malignant tumors. For example ADAM12 has been shown to digest extracellular matrix compounds, gelatin, Type IV collagen and fibronectin.…”

Section: Discussionmentioning

confidence: 99%

TCEB1 promotes invasion of prostate cancer cells

Jalava

Porkka

Rauhala

et al. 2008

Intl Journal of Cancer

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Amplification of the long arm of chromosome 8 is one of the most recurrent findings in prostate cancer and it is associated with poor prognosis. Several minimal regions of amplification suggest multiple target genes which are yet to be identified. We have previously shown that TCEB1, EIF3S3, KIAA0196 and RAD21 are amplified and overexpressed in prostate cancer and they are located in the 8q area. In this study, we examined the functional effects of these genes to prostate cancer cell phenotype. We overexpressed and inhibited the genes by lentivirus mediated overexpression and RNA interference, respectively. shRNA mediated TCEB1 silencing decreased significantly cellular invasion of PC-3 and DU145 cells through Matrigel. TCEB1 silencing reduced the anchorage-independent growth of PC-3 cells. Similar effects were not seen with any other genes. When overexpressed in NIH 3T3 cells, TCEB1 and EIF3S3 increased the growth rate of the cells. Transcriptional profiling of TCEB1 silenced PC-3 cells revealed decrease of genes involved in invasion and metastasis. Finally, we also confirmed here the overexpression of TCEB1 in hormone-refractory prostate tumors. This study indicates that TCEB1 promotes invasion of prostate cancer cells, is involved in development of hormonerefractory prostate cancer and is thereby a strong candidate to be one of the target genes for the 8q gain. ' 2008 Wiley-Liss, Inc.Key words: prostatic carcinoma; RNAi; elongin C Prostate cancer is the most common male malignancy in Western countries and the second most common cause of cancer related deaths in males.1 Because of the intensive research in the past years main chromosomal aberrations in prostate cancer have been revealed, but hunting for many of the target genes is still in process. Gain of the long arm of chromosome 8 (8q) is one of the most recurrent findings in advanced prostate tumors and it is associated with poor prognosis. 2,3Several minimal regions of amplification of 8q have been identified by comparative genomic hybridization (CGH) and array-CGH, suggesting several target genes. Two of these minimal regions are 8q21 and 8q23-24. [4][5][6] We have identified 4 genes that are amplified and highly expressed in prostate cancer and located in these regions. One of them, TCEB1 [transcription elongation factor B (SIII), polypeptide 1 (15 kDa, elongin C)] is located in 8q21.11 and others RAD21 [RAD21 homolog (S. pombe)], KIAA0196 and EIF3S3 (eukaryotic translation initiation factor 3, subunit H) in 8q23-24. 7-9TCEB1 was found to be amplified in 20% of hormone-refractory prostate tumors. Although in untreated primary tumors no gene amplification was found, low-level gains were found in about 30% of the tumors. In PC-3 cell line, which contains the TCEB1 gene amplification, the expression is 5 times higher compared to cell lines with no amplification.7 RAD21 is amplified in 30% of hormone-refractory carcinomas and it is expressed significantly more in untreated prostate carcinomas than in benign prostate hyperplasia (BPH). Also KIAA0196 is amp...

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BNF-1, a novel gene encoding a putative extracellular matrix protein, is overexpressed in tumor tissues

Cited by 19 publications

References 13 publications

Overexpression of colorectal cancer oncogene CHRDL2 predicts a poor prognosis

Overexpression of colorectal cancer oncogene CHRDL2 predicts a poor prognosis

Recurrent genomic alterations in sequential progressive leukoplakia and oral cancer: drivers of oral tumorigenesis?

TCEB1 promotes invasion of prostate cancer cells

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