NF-κB suppression provokes the sensitization of hormone-resistant breast cancer cells to estrogen apoptosis

Lobanova, Yulia S.; Scherbakov, Alexander M.; Shatskaya, V. A.; Евтеев, В. А.; Красильников, М. А.

doi:10.1007/s11010-008-9985-0

Cited by 16 publications

(12 citation statements)

References 15 publications

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“…These sex differences implicate estrogens as potentially protective, or indicate that androgens may aggravate NASH. Estrogen has been shown to be anti-apoptotic and anti-fibrogenic in in vitro studies in various cancer cell lines (18) and in in vivo studies in rats and geese (19). Estrogen, especially 4-hydroxy estrone, reduces lipid peroxidation in lipoproteins or whole plasma by reducing the levels of both lipid (thiobarbituric acid-reactive substances) and cholesterol (oxysterols) oxidation products and thereby leads to reduced reactive oxygen species (20).…”

Section: Definitions and Epidemiologymentioning

confidence: 99%

Advances in Pediatric Nonalcoholic Fatty Liver Disease†

et al. 2009

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Nonalcoholic fatty liver disease (NAFLD) has emerged as the leading cause of chronic liver disease in children and adolescents in the United States. A two-to three-fold rise in the rates of obesity and overweight in children over the last two decades is probably responsible for the NAFLD epidemic. Emerging data suggest that children with nonalcoholic steatohepatitis (NASH) progress to cirrhosis, which may ultimately increase liver-related mortality. More worrisome is the recognition that cardiovascular risk and morbidity in children and adolescents are associated with fatty liver. Pediatric fatty liver disease often displays a histologic pattern distinct from that found in adults. Liver biopsy remains the gold standard for diagnosis of NASH. Noninvasive biomarkers are needed to identify individuals with progressive liver injury. Targeted therapies to improve liver histology and metabolic abnormalities associated with fatty liver are needed. Currently, randomized-controlled trials are underway in the pediatric population to define pharmacologic therapy for NAFLD. Public health awareness and intervention are needed to promote healthy diet, exercise, and lifestyle modifications to prevent and reduce the burden of disease in the community. (HEPATOLOGY 2009;50:1282-1293

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Section: Definitions and Epidemiologymentioning

confidence: 99%

Advances in Pediatric Nonalcoholic Fatty Liver Disease†

et al. 2009

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“…The cell lines were used as follows: (1) ER-positive (high ER level) estrogen-dependent MCF-7 cells, (2) ER-positive estrogen-hyposensitive MCF-7/LS subline generated through 2-month cultivation of the parental cells in steroid-free medium [Lobanova et al, 2009], (3) ER-negative estrogen-independent HBL-100 cells.…”

Section: The Expression and Activity Of Snail1 In Different Breast Camentioning

confidence: 99%

The relationships between snail1 and estrogen receptor signaling in breast cancer cells

Scherbakov

Andreeva

Shatskaya

et al. 2012

J of Cellular Biochemistry

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The loss of hormonal dependency of breast tumor cells is often accompanied with the appearance of epithelial-mesenchymal transition (EMT) features and increase in cell metastasis and invasiveness. The central role in the EMT belongs to transcription factors Snail responded for the decrease in E-cadherin expression and cell contacts, stimulation of cell mobility and invasiveness. Aim was to study the relationships between estrogen receptor machinery and Snail1 signaling, and mechanism of Snail1 regulation in hormone-resistant breast cancer cells. The experiments were performed on the estrogen-dependent MCF-7 breast cancer cells, estrogen-hyposensitive MCF-7/LS subline generated through long-term cultivation of the parental cells in steroid-free medium, and ER-negative estrogen-resistant HBL-100 cells. Snail1, estrogen receptor, p65 NF-κB, E-cadherin levels were analyzed by Western blot. We found that decrease in the estrogen dependency is correlated with increase in Snail1 expression and activity, we demonstrated the Snail1 involvement in the negative regulation of ER, and showed that Snail1 inhibition partially restores the sensitivity of the estrogen-hyposensitive cells to antiestrogen tamoxifen. Furthermore, NF-κB was found to serve as a positive regulator of Snail1 in breast cancer cells, and simultaneous inhibition of NF-κB and Snail1 resulted in additional increase in cell response to tamoxifen. In general, the results obtained demonstrate the phenomenon of Snail1 activation in the hormone-resistant breast cancer cells, and show that Snail1 and NF-κB may serve as an important targets in the treatment of breast cancer, both estrogen-dependent and estrogen-independent tumors.

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“…It is possible to hypothesize that estrogens can be potentially liver-protective; or indicate that androgens may aggravate NASH [38,39]. …”

Section: Introductionmentioning

confidence: 99%

Pediatric non alcoholic fatty liver disease: old and new concepts on development, progression, metabolic insight and potential treatment targets

et al. 2013

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Nonalcoholic fatty liver disease (NAFLD) is the leading cause of chronic liver disease in children. NAFLD has emerged to be extremely prevalent, and predicted by obesity and male gender. It is defined by hepatic fat infiltration >5% hepatocytes, in the absence of other causes of liver pathology. It includes a spectrum of disease ranging from intrahepatic fat accumulation (steatosis) to various degrees of necrotic inflammation and fibrosis (non-alcoholic steatohepatatis [NASH]). NAFLD is associated, in children as in adults, with severe metabolic impairments, determining an increased risk of developing the metabolic syndrome. It can evolve to cirrhosis and hepatocellular carcinoma, with the consequent need for liver transplantation. Both genetic and environmental factors seem to be involved in the development and progression of the disease, but its physiopathology is not yet entirely clear. In view of this mounting epidemic phenomenon involving the youth, the study of NAFLD should be a priority for all health care systems. This review provides an overview of current and new clinical-histological concepts of pediatric NAFLD, going through possible implications into patho-physiolocical and therapeutic perspectives.

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NF-κB suppression provokes the sensitization of hormone-resistant breast cancer cells to estrogen apoptosis

Cited by 16 publications

References 15 publications

Advances in Pediatric Nonalcoholic Fatty Liver Disease†

Advances in Pediatric Nonalcoholic Fatty Liver Disease†

The relationships between snail1 and estrogen receptor signaling in breast cancer cells

Pediatric non alcoholic fatty liver disease: old and new concepts on development, progression, metabolic insight and potential treatment targets

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