Lipocalins and cancer

Bratt, Tomas

doi:10.1016/s0167-4838(00)00154-0

Cited by 118 publications

(111 citation statements)

References 47 publications

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“…Lipocalins are extracellular carriers of lipophilic molecules, such as retinoids, steroids and fatty acids, all of which may play important roles in the regulation of epithelial cell growth. 51,52 In addition, because lipocalin is a secreted protein, it may play a role in the regulation of cell proliferation and survival. 51,52 Of interest, 2 publications, on gene expression profiling of breast and pancreatic cancers, have proposed lipocalin 2 as a novel therapeutic and diagnostic marker for prevention and treatment of these diseases.…”

Section: Discussionmentioning

confidence: 99%

“…51,52 In addition, because lipocalin is a secreted protein, it may play a role in the regulation of cell proliferation and survival. 51,52 Of interest, 2 publications, on gene expression profiling of breast and pancreatic cancers, have proposed lipocalin 2 as a novel therapeutic and diagnostic marker for prevention and treatment of these diseases. 53,54 On the basis of our findings, lipocalin 2 may be added to the known markers for ovarian cancer.…”

Section: Discussionmentioning

confidence: 99%

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Gene expression profiles in primary ovarian serous papillary tumors and normal ovarian epithelium: Identification of candidate molecular markers for ovarian cancer diagnosis and therapy

Santin

Zhan

Bellone

et al. 2004

Intl Journal of Cancer

264

187

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Gene expression profiles in primary ovarian serous papillary tumors and normal ovarian epithelium: Identification of candidate molecular markers for ovarian cancer diagnosis and therapy

Santin

Zhan

Bellone

et al. 2004

Intl Journal of Cancer

264

187

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“…Persistent pulmonary inflammation in Rosa26-Foxm1 lungs was associated with increased expression of Lipocalin-2, the CXC chemokine ligand 5 (CXCL5), CXCL1, and the CC chemokine ligand 3 (CCL3) (Figure 3), all of which stimulate signaling pathways essential for pulmonary inflammation and lung remodeling (Bratt, 2000;Kulbe et al, 2004). Interestingly, by 24 weeks after tumor initiation, expression levels of these genes were decreased in the Rosa26-Foxm1 lungs to approximately WT levels ( Figure 3).…”

Section: Foxm1 Induces Formation Of Lung Tumors I-c Wang Et Almentioning

confidence: 99%

Transgenic expression of the forkhead box M1 transcription factor induces formation of lung tumors

et al. 2008

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The forkhead box m1 (Foxm1 or Foxm1b) protein (previously called HFH-11B, Trident, Win or MPP2) is abundantly expressed in human non-small cell lung cancers where it transcriptionally induces expression of genes essential for proliferation of tumor cells. In this study, we used Rosa26-Foxm1 transgenic mice, in which the Rosa26 promoter drives ubiquitous expression of Foxm1 transgene, to identify new signaling pathways regulated by Foxm1. Lung tumors were induced in Rosa26-Foxm1 mice using the 3-methylcholanthrene (MCA)/butylated hydroxytoluene (BHT) lung tumor initiation/promotion protocol. Tumors from MCA/BHTtreated Rosa26-Foxm1 mice displayed a significant increase in the number, size and DNA replication compared to wild-type mice. Elevated tumor formation in Rosa26-Foxm1 transgenic lungs was associated with persistent pulmonary inflammation, macrophage infiltration and increased expression of cyclooxygenase-2 (Cox-2), Cdc25C phosphatase, cyclin E2, chemokine ligands CXCL5, CXCL1 and CCL3, cathepsins and matrix metalloprotease-12. Cell culture experiments with A549 human lung adenocarcinoma cells demonstrated that depletion of Foxm1 by either short interfering RNA transfection or treatment with Foxm1-inhibiting ARF 26-44 peptide significantly reduced Cox-2 expression. In co-transfection experiments, Foxm1 protein-induced Cox-2 promoter activity and directly bound to the À2566/ À2580 bp region of human Cox-2 promoter.

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“…The augmented MMP1 transcription in FUS-DDIT3-expressing cells probably results from a different mechanism. Elevated expressions of MMP1 and LCN2 have been reported to be associated with advanced cancers, metastasis and invasiveness (Nakopoulou et al, 1999;Bratt, 2000;Brinckerhoff et al, 2000), suggesting a role for these genes also in the development of MLS/RCLS.…”

Section: Fus-ddit3 Deregulates Nf-jb Target Genesmentioning

confidence: 99%

The myxoid liposarcoma FUS-DDIT3 fusion oncoprotein deregulates NF-κB target genes by interaction with NFKBIZ

et al. 2008

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FUS (also called TLS), EWSR1 and TAF15 (also called TAF2N) are related genes involved in tumor type-specific fusion oncogenes in human malignancies. The FUS-DDIT3 fusion oncogene results from a t(12;16)(q13;p11) chromosome translocation and has a causative role in the initiation of myxoid/round cell liposarcomas (MLS/ RCLS). The FUS-DDIT3 protein induces increased expression of the CAAT/enhancer-binding protein (C/EBP) and nuclear factor-jB (NF-jB)-controlled gene IL8, and the N-terminal FUS part is required for this activation. Chromatin immunoprecipitation analysis showed that FUS-DDIT3 binds the IL8 promoter. Expression studies of the IL8 promoter harboring a C/EBP-NF-jB composite site pinpointed the importance of NF-jB for IL8 expression in FUS-DDIT3-expressing cells. We therefore probed for possible interaction of FUS-DDIT3 with members of the NF-jB family. The nuclear factor NFKBIZ colocalizes with FUS-DDIT3 in nuclear structures, and immunoprecipitation experiments showed that FUS-DDIT3 binds the C-terminal of NFKBIZ. We also report that additional NF-jB-controlled genes are upregulated at the mRNA level in FUS-DDIT3-expressing cell lines and they can be induced by NFKBIZ. Taken together, the results indicate that FUS-DDIT3 deregulates some NF-jB-controlled genes through interactions with NFKBIZ. Similar mechanisms may be a part of the transformation process in other tumor types carrying FUS, EWSR1 and TAF15 containing fusion oncogenes.

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Lipocalins and cancer

Cited by 118 publications

References 47 publications

Gene expression profiles in primary ovarian serous papillary tumors and normal ovarian epithelium: Identification of candidate molecular markers for ovarian cancer diagnosis and therapy

Gene expression profiles in primary ovarian serous papillary tumors and normal ovarian epithelium: Identification of candidate molecular markers for ovarian cancer diagnosis and therapy

Transgenic expression of the forkhead box M1 transcription factor induces formation of lung tumors

The myxoid liposarcoma FUS-DDIT3 fusion oncoprotein deregulates NF-κB target genes by interaction with NFKBIZ

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