Apoptosis induced by uterine 24p3 protein in endometrial carcinoma cell line

Lin, Hsiu Hsia; Li, Wen-Wei; Lee, Ying-Chu; Chu, Shao‐I

doi:10.1016/j.tox.2007.02.017

Cited by 31 publications

(30 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It has been shown previously that LCN2 increases the sensitivity of glial cells to apoptotic as well as necrotic stimuli ). LCN2 also induces ROS-mediated apoptosis in an endometrial carcinoma cell line (Lin et al, 2007). Increased expression of LCN2 has been linked to the induction of apoptosis in F12.5 murine lymphocytes and L929 fibroblasts (Devireddy et al, 2005;.…”

Section: Discussionmentioning

confidence: 98%

Regulation by lipocalin‐2 of neuronal cell death, migration, and morphology

Lee

et al. 2011

J of Neuroscience Research

View full text Add to dashboard Cite

A secreted protein, lipocalin-2 (LCN2), has been previously shown to regulate a variety of cellular phenotypes such as cell death, migration, and morphology. The role of LCN2, however, appears to be different depending on the cellular context. Here, we investigated how LCN2 influences neuronal phenotypes by using primary cortical neuronal cell cultures and neuroblastoma cell lines as a model. When exposed to LCN2 protein, neurons and neuroblastoma cells were sensitized to cell death evoked by nitric oxide, oxidative stress, and tumor necrosis factor-α (TNF-α). A forced expression of lcn2 in glia enhanced neuronal cell death in cocultures of glia and neurons, indicating that both exogenous protein addition and endogenous expression of lcn2 give rise to similar results. Iron and BCL2-interacting mediator of cell death (BIM) protein were involved in LCN2-induced cell death sensitization, based on the studies using iron donor, chelator, siderophore, and short hairpin RNA (shRNA)-mediated knockdown of bim expression. Furthermore, cell migration assay and immunofluorescence microscopic observation revealed that LCN2 accelerated neuronal motility and process extension, suggesting multiple roles for LCN2 in the regulation of neuronal cell death, migration, and morphology.

show abstract

Section: Discussionmentioning

confidence: 98%

Regulation by lipocalin‐2 of neuronal cell death, migration, and morphology

Lee

et al. 2011

J of Neuroscience Research

View full text Add to dashboard Cite

show abstract

“…Intriguingly, NGAL localization was remarkably similar to the distribution of TUNEL staining, suggesting that NGAL may be responsible for mediating the apoptotic effect of 13-cis RA on sebaceous glands. Increased expression of LCN2 has been linked with the induction of apoptosis in endometrial carcinoma, F12.5 murine lymphocytes, and L929 fibroblasts (6,33,34). Using immunohistochemistry, NGAL expression was increased by only 1% in female skin compared with 12%-36% in male patients, suggesting possible gender differences in NGAL protein expression in response to 13-cis RA.…”

Section: Discussionmentioning

confidence: 99%

Neutrophil gelatinase–associated lipocalin mediates 13-cis retinoic acid–induced apoptosis of human sebaceous gland cells

Nelson¹,

Zhao²,

Gilliland³

et al. 2008

J. Clin. Invest.

130

141

View full text Add to dashboard Cite

13-cis retinoic acid (13-cis RA; also known as isotretinoin) is the most potent agent available for treatment of acne. It is known that the drug induces apoptosis in cells cultured from human sebaceous glands, but its mechanism of action has not been determined. In this study, skin biopsies were taken from 7 patients with acne prior to and at 1 week of treatment with 13-cis RA. TUNEL staining confirmed that 13-cis RA induced apoptosis in sebaceous glands. Transcriptional profiling of patient skin and cultured human sebaceous gland cells (SEB-1 sebocytes) indicated that lipocalin 2 was among the genes most highly upregulated by 13-cis RA. Lipocalin 2 encodes neutrophil gelatinase-associated lipocalin (NGAL), which functions in innate immune defense and induces apoptosis of murine B lymphocytes. Increased immunolocalization of NGAL was noted in patients' sebaceous glands following treatment with 13-cis RA, and recombinant NGAL induced apoptosis in SEB-1 sebocytes. Furthermore, apoptosis in response to 13-cis RA was inhibited in the presence of siRNA to lipocalin 2. These data indicate that NGAL mediates the apoptotic effect of 13-cis RA and suggest that agents that selectively induce NGAL expression in sebaceous glands might represent therapeutic alternatives to the use of 13-cis RA to treat individuals with acne.

show abstract

“…LCN2 is an estrogen-dependent, acute-phase protein that in mice has been implicated in multiple processes, including apoptosis, ion transport, inflammation, cell survival, and tumorigenesis (Chu et al 1996, Liu et al 1997, Lin et al 2007. As mentioned earlier, LCN2 is upregulated in the endometriotic lesions (Konno et al 2007, Becker et al 2010.…”

Section: Introductionmentioning

confidence: 86%

“…As LCN2 is a stress protein (Lin et al 2007), we used a 1% FBS culture medium, which causes nutrient-deprivation stress, to induce LCN2 production. We then characterized physiological changes to primary endometrial epithelial cells.…”

Section: Emt Of Primary Endometrial Epithelial Cells Cultured In Nutrmentioning

confidence: 99%

Lipocalin 2 induces the epithelial–mesenchymal transition in stressed endometrial epithelial cells: possible correlation with endometriosis development in a mouse model

Liao

Lee

et al. 2014

Reproduction

Self Cite

View full text Add to dashboard Cite

Lipocalin 2 (LCN2) is an induced stressor that promotes the epithelial-mesenchymal transition (EMT). We previously demonstrated that the development of endometriosis in mice correlates with the secretion of LCN2 in the uterus. Here, we sought to clarify the relationship between LCN2 and EMT in endometrial epithelial cells and to determine whether LCN2 plays a role in endometriosis. Antibodies that functionally inhibit LCN2 slowed the growth of ectopic endometrial tissue in a mouse model of endometriosis, suggesting that LCN2 promotes the formation of endometriotic lesions. Using nutrient deprivation as a stressor, LCN2 expression was induced in cultured primary endometrial epithelial cells. As LCN2 levels increased, the cells transitioned from a round to a spindle-like morphology and dispersed. Immunochemical analyses revealed decreased levels of cytokeratin and increased levels of fibronectin in these endometrial cells, adhesive changes that correlate with induction of cell migration and invasion. Lcn2 knockdown also indicated that LCN2 promotes EMT and migration of endometrial epithelial cells. Our results suggest that stressful cellular microenvironments cause uterine tissues to secrete LCN2 and that this results in EMT of endometrial epithelial cells, which may correlate with the development of ectopic endometriosis. These findings shed light on the role of LCN2 in the pathology of endometrial disorders.

show abstract

Apoptosis induced by uterine 24p3 protein in endometrial carcinoma cell line

Cited by 31 publications

References 51 publications

Regulation by lipocalin‐2 of neuronal cell death, migration, and morphology

Regulation by lipocalin‐2 of neuronal cell death, migration, and morphology

Neutrophil gelatinase–associated lipocalin mediates 13-cis retinoic acid–induced apoptosis of human sebaceous gland cells

Lipocalin 2 induces the epithelial–mesenchymal transition in stressed endometrial epithelial cells: possible correlation with endometriosis development in a mouse model

Contact Info

Product

Resources

About