Lipocalin 2 is required for BCR-ABL-induced tumorigenesis

Leng, Xiaohong; Lin, Hui Kuan; Tian, Di; Wang, Y; Wu, Yun; Klumpp, Sherry A.; Sun, Tong; Zhou, Yanxiang; Monaco, Paola; Belmont, John W.; Aderem, Alan; Akira, Shizuo; Strong, Roland K.; Arlinghaus, Ralph B.

doi:10.1038/onc.2008.209

Cited by 83 publications

(95 citation statements)

References 26 publications

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“…This mechanism has been suggested to be responsible for the spread of leukemia cells through the healthy bone marrow. [12][13][14] Studies in CML patients have confirmed the findings in mice. Both NGAL mRNA and plasma levels are significantly elevated in patients with CML.…”

Section: Introductionsupporting

confidence: 66%

“…Both NGAL mRNA and plasma levels are significantly elevated in patients with CML. 12,15 Further, patients who responded to treatment with Imatinib (a specific inhibitor of BCR-ABL tyrosine kinase) showed a significant decrease in NGAL mRNA. 16 The present study was conducted to evaluate the status of NGAL in CML patients before and after chemotherapy and also to compare the NGAL values in remission and non-remission CML patients.…”

Section: Introductionmentioning

confidence: 99%

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Neutrophil gelatinase-associated lipocalin (NGAL) as a prognostic marker in chronic myeloid Leukemia: an observational study

Mehta¹,

Rohilla

Rohila

2017

Int J Res Med Sci

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Background: Neutrophil gelatinase-associated lipocalin (NGAL) is a protein which is associated with various inflammatory conditions affecting human tissues, such as those in the respiratory, gastro-enteric and urinary tracts, with a marked increase in the local and systemic expression. Different experimental evidences reveal that NGAL is required for the induction and pathogenesis of chronic myeloid leukemia (CML).Methods: The present study was conducted in department of Biochemistry in a tertiary care institute of Haryana. 30 cases of CML were included in the study. It was a hospital based observational study which was conducted for one-year duration. Apart from routine biochemical investigations, serum NGAL estimation was done before the initiation of therapy and after 3 months of therapy.Results: The median age at presentation was 39 years. Male to female ratio was 1.3:1. Weight loss was the most common presentation of patients (53.3%). More than half of the cases occurred in age group of 21-40 years. Serum NGAL was significantly higher in CML patients (358.47±125.65) before treatment as compared to serum NGAL value after treatment (85.03±62.77). In patients who achieved hematological remission, mean serum NGAL levels (62.46 ng/ml±23.72) were statistically lower than mean serum NGAL values in patients who did not achieve remission (231.75 ng/ml±16.7).Conclusions: The present study concluded that serum NGAL levels can be used as diagnostic and prognostic marker in CML.

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Section: Introductionsupporting

confidence: 66%

Section: Introductionmentioning

confidence: 99%

Neutrophil gelatinase-associated lipocalin (NGAL) as a prognostic marker in chronic myeloid Leukemia: an observational study

Mehta¹,

Rohilla

Rohila

2017

Int J Res Med Sci

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“…Recently, LCN2 has been implicated in tumorigenesis and formation of metastases in murine breast cancer models (Shi et al, 2008;Leng et al, 2009;Yang et al, 2009). A potential function for LCN2 in the migratory capacity of colon cells (Playford et al, 2006) and tissue invasion by leukemia cells (Leng et al, 2008) has also been documented. The LCN2 gene is specifically downregulated in estrogen receptor a positive (ERA þ ) breast cancer patients (Stoesz et al, 1998) and has been reported as a predictor of breast cancer progression (Bauer et al, 2008;Provatopoulou et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

NFAT3 transcription factor inhibits breast cancer cell motility by targeting the Lipocalin 2 gene

et al. 2010

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NFAT1 and NFAT5 act as pro-invasive and promigratory transcription factors in breast carcinoma, contributing to the formation of metastases. We report that NFAT3 is specifically expressed in estrogen receptor a positive (ERA þ ) breast cancer cells. We show that NFAT3 inhibits by itself the invasion capacity of ERA þ breast cancer cells and needs to cooperate with ERA to inhibit their migration. Conversely, NFAT3 downregulation results in actin reorganization associated with increased migration and invasion capabilities. NFAT3 signaling reduces migration through inhibition of Lipocalin 2 (LCN2) gene expression. Collectively, our study unravels an earlier unknown NFAT3/LCN2 axis that critically controls motility in breast cancer.

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“…Alternatively, NGAL has been associated with metastatic stages of tumorigenesis. The role of NGAL in tumor formation may be linked to the fact that NGAL stabilizes the enzymatic activity of MMP-9 (29,30). For example, NGAL was suggested to play an important role in breast cancer by protecting MMP-9 from degradation and thereby favoring tumor invasion (31).…”

Section: Discussionmentioning

confidence: 99%

Identification of gene expression profiles correlated to tumor progression in a preclinical model of colon carcinogenesis

Bousserouel

Kauntz²,

Gossé³

et al. 2010

Int J Oncol

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Abstract. The rat azoxymethane (AOM)-induced colon carcinogenesis model provides useful information for understanding human colorectal neoplasia. Here, we used the AOM model to measure the gene expression profiles of biomarkers related to tumor progression. We assessed tumor progression stages by computed tomographic (CT) colonography. Messenger RNAs were isolated from tumors and mucosal samples, and gene expression levels were assessed by realtime quantitative polymerase chain reaction (PCR). We show that early stages of tumor progression are associated with an upregulation of matrix metalloproteinase-7 (MMP-7) and of genes involved in the inflammatory response, including interleukin (IL1ß) and tumor necrosis factor-· (TNF·). The ratio of B-cell lymphoma/leukemia 2 (Bcl-2)-associated X proteins (Bax) to Bcl-2 transcript (proapototic/antiapoptotic signals) is elevated in early stages of tumor progression (Bax/Bcl-2 >1) and reversed in more advanced stages of tumor development (Bax/Bcl-2 <1). These changes are associated with the reduced expression of TNF-related apoptosis-inducing ligand (TRAIL)-death receptor 5 (DR5) and FAS (also known as CD95) apoptotic receptors. Advanced stages of tumor development are characterized by an increase in MMP-9 expression associated with the upregulation of components of the innate immune system: ·-defensin 5 (DEF-5) and neutrophil gelatinaseassociated lipocalin (NGAL). The identification of specific gene expression profiles that correlate with tumor progression stages, as reported in the present study, may represent an important step in evaluating potential chemopreventive and/ or chemotherapeutic agents prior to initiating clinical trials.

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Lipocalin 2 is required for BCR-ABL-induced tumorigenesis

Cited by 83 publications

References 26 publications

Neutrophil gelatinase-associated lipocalin (NGAL) as a prognostic marker in chronic myeloid Leukemia: an observational study

Neutrophil gelatinase-associated lipocalin (NGAL) as a prognostic marker in chronic myeloid Leukemia: an observational study

NFAT3 transcription factor inhibits breast cancer cell motility by targeting the Lipocalin 2 gene

Identification of gene expression profiles correlated to tumor progression in a preclinical model of colon carcinogenesis

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