n represents the number of indie experiments. glucose incubation significantly decreased apoptosis and necrosis, while increasing viability in both cell lines in a dose dependent manner. One-hour leptin treatment significantly decreased viability, and increased apoptosis but did not significantly impact necrosis in T47D cells incubated in 2.5 mM glucose. In MCF-7 cells, one-hour leptin incubation significantly increased necrosis but its effects on apoptosis and viability were not significant. In conclusion, although glucose induces cell death by apoptosis and necrosis in T47D and MCF-7 cells respectively in a dose dependent manner, the overallviability is still increased in both cell lines. One-hour leptin treatment reverses the effect of low glucose incubation on apoptosis of T47D and necrosis of MCF-7 cells. Moreover, the effect of one-hour leptin treatment on apoptosis or necrosis is usually significantly higher than that of 24-hour leptin treatment. Keywords: Calorie restriction, Malignancy cell viability, Glucose, Leptin, MCF-7, T47D 1.?Introduction Breast cancer is Ritonavir the most commonly diagnosed malignancy and the second leading cause of cancer related death among women worldwide (Niu et al., 2013). Ritonavir A number of meta-analyses revealed that obesity and body weight (BW) gain are associated with an increased breast cancer risk, especially for post-menopausal women (Keum et al., 2015). Obesity has been reported to be related to an increased risk of disease recurrence (Ligibel, 2011) and a poorer survival rate (Chan et al., 2014) in both pre- and post-menopausal women diagnosed with breast cancer. Although there are several previous studies investigating the association between obesity and breast malignancy development, the molecular mechanism of the association remains largely unknown (Dogan et al., 2007; Dogan et al., 2011; Tuna et al., 2017). In this context, adipokines are suggested as important molecules linking obesity to breast malignancy (Dogan et al., 2010; Cicekdal et al., 2019; Cicekdal et al., 2019). Leptin, a 16 kDa peptide hormone, is an adipokine secreted mainly by the adipose tissue as a product of the obese (Ob) gene. There is a well-established link between leptin and obesity (Artac and Altundag, 2012) as leptin is usually a key appetite-regulating hormone which plays critical functions in appetite control, energy intake and energy expenditure (Amitani et al., 2013). Both leptin and its receptors were reported to be overexpressed in breast cancer tissue (Ishikawa et al., 2004). Consistently, serum leptin levels have also been reported to be significantly higher in breast cancer patients compared to that of healthy individuals (Wu et al., 2009). Besides, circulating leptin levels are higher in breast cancer patients with lymph node metastasis relative to the benign disease breast cancer patients (Niu et al., 2013). Effects of leptin around the proliferation and survival of anchorage impartial growth of breast cancer cells have also been exhibited in vitro (Hu et al., 2002). Calorie restriction, defined as reducing the energy intake without causing malnutrition, is one of the most accepted preventive methods for breast cancer development in many species (Dogan et al., 2010; OFlanagan et al., 2017). In vitro cell culture models may allow for a more controllable calorie intake and also provide quantification of inputs and outputs on a molecular level in a shorter period of time. Therefore, in vitro cell culture experimental design of calorie intake (lower or higher), which is usually controlled by the glucose concentration in cell culture, may lead to a better understanding of the association between leptin and breast malignancy cell proliferation. Leptin plays an important role in the regulation of glucose metabolism impartial of its effect on BW. Inadequate leptin signaling has a pivotal role in hyperglycemia Ritonavir induction, persistence of which may lead to diabetes (Amitani et al., 2013). Consistently, chronic hyperglycemia is usually a common characteristic of mice lacking the leptin encoding gene (ob/ob) (Dsouza et al., 2017) and is alleviated by administration of low doses of leptin that do not significantly impact BW in ob/ob mice (Pelleymounter et al., 1995; Hedbacker et al., 2010). However, not much is known about the effect of leptin around the viability and Mouse monoclonal to CK17 mode of cell death in breast cancer cells especially in the presence of different glucose concentrations in-vivo or in vitro. Here, we investigated the effect of leptin on viability and cell death using MCF-7 and T47D breast malignancy cell lines cultured in different glucose concentrations (0 mM, 2.5 mM, 5 mM (normal glucose levels in cell medium), 25 mM, 50 mM), which mimics in-vivo calorie intake conditions (lower or higher) in-vitro condition. The present study is the continuation of our previous research which was focusing on the.
n represents the number of indie experiments