Caspases activities in TNF-α applied HepG2 hepatocellular carcinoma cell

Amaç: Tümör nekroz faktörü (TNF), hücre sağkalımı, proliferasyon, farklılaşma, inflamasyon, bağışıklık ve apoptoz gibi hücresel olaylarda anahtar rol oynar. Tümör sitotoksisitesindeki etkisinden dolayı Tümör nekroz faktörü olarak adlandırılmasına rağmen, TNF geniş bir yelpazede birçok hastalıkla ilişkilendirilmiştir. Çalışmada, hepatoselüler karsinoma hücrelerinde TNF-α'nın kaspaz 1, 3 ve 9 enzim aktiviteleri üzerindeki etkilerini belirlemek amaçlanmıştır. Materyal ve metod: Çalışmada TNF-α uygulanmayan (kontrol) ve 24 saat boyunca TNF-α uygulanan hepatoselüler karsinoma hücre hattı HepG2 hücreleri kullanılmıştır. TNF-α'nın kaspaz 1, kaspaz 3 ve kaspaz 9 enzim aktiviteleri üzerindeki etkileri kolorimetrik olarak ticari kit ile gerçekleştirilmiştir. Bulgular: TNF-α uygulanan HepG2 hücrelerinde kaspaz 1 ve kaspaz 3 enzim aktivitelerinde kontrol grubuna göre anlamlı artış gözlenmiştir (p<0,05). Sonuç: TNF-α inflamatuar hücreler tarafından salınan pro-inflamatuvar bir sitokindir. Bu mekanizma, yangıya bağlı şekillenen karsinogenezde rol oynayabilir. TNF, hem tümör oluşumunu destekleyebilir hem de kanser hücrelerini öldürücü etki gösterebilir. Sunulan bulgular, TNF-α uygulanan HepG2 hücrelerinde kaspaz bağlımlı hücre ölümünün meydana geldiğini ortaya koymaktadır.Purpose: Tumor necrosis factor (TNF) plays a key role in cellular events such as cell survival, proliferation, differentiation, inflammation, immunity, and apoptosis. Although named Tumor necrosis factor for its tumor cytotoxicity, TNF has been implicated in a wide spectrum of other diseases. The aim of the present study is to determine the effects of TNF-α on caspase 3, 9, and 1 enzyme activities in HepG2 cells. Materials and methods: Hepatocellular carcinoma cell line HepG2 was used and cells were cultured in the absence (control) or presence of TNF-α for 24 h. The effect of TNF-α on caspase 3, caspase 9, and caspase 1 enzyme activities in hepatocarcinoma cells were examined in TNF-α treated and control cells using colorimetric assay kits. Results: There were significant increases in caspases 1 and 3 levels in TNF-α treated HepG2 cells compare to control cells. Conclusions: TNF-α is a pro-inflammatory cytokine, secreted by inflammatory cells. This mechanism may be involved in inflammation-associated carcinogenesis. TNF could act both as tumor promoter, and cancer killer. Presented findings suggest that caspases-dependent cell death occurs in TNF-α applied HepG2 cells

The investigation antiproliferative and apoptotic effects of capsaicin and alpha lipoic acid on colon adenocarcinoma cells

WOS: 000431624200026

Antioxidant therapy impresses in oxidative stress-induced kidney cells

Meral, Ogunc/0000-0001-8813-4991WOS: 000395357800005PubMed: 28814089INTRODUCTION: Renal cell cancer (RCC) is not a single entity, but consists of different types of tumors derived from various parts of the nephron (epithelium or renal tubules). It is known that cancer initiation and progression is related to the balance between oxidants and antioxidants directly. Interestingly, advanced stages of cancer such as metastasis, angiogenesis are associated with cell oxidative capacity. Familiar antioxidative substances such as carotenes and vitamin C inhibit oxidation of other molecules during carcinogenesis. They can define the distinction between cancer and normal cells, destroying cancer cells while stabilizing healthy cells. METHODS: apoptotic activities of kidney cells were measured with caspase Elisa kits. DNA laddering test was used to show DNA damage in H2O2 condition. RESULTS: For tumor mechanism, they act as pro-oxidants, producing hydrogen peroxide that attacks the cancer, whereas, in normal conditions they act as protective antioxidants. CONCLUSIONS: The unlike reaction of specific antioxidants should be known at different cell stages. The aim of this study was to assess the antioxidative roles of alpha lipoic acid on kidney cancers during oxidative stress induction (Tab. 1, Fig. 7, Ref 27). Text in PDF www.elis.sk

The Effect of Tocopherol-α on the Cell Viability in Caco-2 Cell Line

Tocopherols, the major forms of vitamin E, are a family of fat-soluble phenolic compounds. Each tocopherol contains a chromanol ring system and a phytyl chain containing 16 carbons. Tocopherols, as effective antioxidants, have been proposed to protect against carcinogenesis. Colon carsinoma cell line were treated with tocopherol-α (0, 3.12, 6.25, 12.5, 25, 50, 100, 200 uM). Cell viability and migration were examined. Cell viability was determined MTT assay and cell migration was determined by wound healing assay. Caco-2 cells were treated with for 24 h, 48 h and 72 h incubation. There is a significant decrease was observed at 50, 100 and 200 µM for 48 h and 72 h incubation on cell viability in the MTT assay. Wound healing method observed decrease on migration at 12, 5, 25 and 50 µM in 24 h. These results suggest that tocopherol-α have promising antiproliferative effect on cell viability for research on cancer

The Antiproliferative Effect of Alpha Tocopherol in F98 Cell Culture

Alpha tocopherol is the most common and biologically active form of Vitamin E. The aim of this study was to evaulate the possible antiproliferative effect of alpha tocopherol on F-98 Glioblastoma cells. F-98 glioblastoma cell line was seeded at a density of 50.000/mL per well in 96 well plates in 100 µL medium DMEM. Cells treated with Alpha tocopherol (200,100, 50, 25, 12.5, 6.2, 3.3 µM) for 24 h, 48 h and 72 h incubation. Measurement of Alpha tocopherol treated and control groups’ cell proliferation performed with MTT assay and Wound Healing assay was employed to show migration capacity. MTT Assay data shown are there was significant change in cell viability in 24 h, 48 h and 72 h. However significant decrease was observed at 50, 100 and 200 µM. In the present study, antiproliferative effect of alpha tocopherol was observed via wound healing assay. Our results here show that Alpha Tocopherol maybe a possible avenue for brain cancer treatment

In Vitro Effects of Phthalate Mixtures on Colorectal Adenocarcinoma Cell Lines

KUZUKIRAN, OZGUR/0000-0001-9294-2801; Filazi, Ayhan/0000-0002-2800-6215WOS: 000368384400003PubMed: 26081030Among endocrine-disrupting chemicals, phthalates are an important concern because of their widespread exposure in humans and environmental contamination. Even though the use of some phthalates has been restricted for toys, some plastics, and food contact materials, exposure to the mixture of these contaminants at very low concentrations in various matrices are still being reported. In the current research, the effects of the mixture of some phthalates were studied. Di-n-butyl phthalate (DBP), n-butyl benzyl phthalate (BBP), di-2-ethylhexyl phthalate (DEHP), diisononyl phthalate (DiNP), di-n-octyl phthalate (DNOP), and diisodecyl phthalate (DiDP) were tested on two colorectal adenocarcinoma cell lines; DLD-1 and HT29 were studied as described before. Cells were treated with increasing log concentrations (0.33 ppt to 33.33 ppb) of the phthalate mixture, cell viability/proliferation was measured by MTT and staining with neutral red and crystal violet; lactate dehydrogenase (LDH) activity was measured following 24-h exposure. Cell viability/proliferation increased from phthalate treatment at concentrations less than 33.33 ppt. The phthalate mixture induced increases in HT29 proliferation of 10.94% at 33.33 ppt and 60.87% at 3.33 ppt, whereas this proliferation relation at lower concentrations was not found for DLD1 cells. The present study demonstrates preliminary information regarding the low dose induction of proliferation of the cancer cells by phthalate mixtures. Because non-monotonic dose responses are still being debated, further studies are required to re-evaluate the reference doses defined by governments for phthalates

GSM-like radiofrequency exposure induces apoptosis via caspase-dependent pathway in infant rabbits

Meral, Ogunc/0000-0001-8813-4991WOS: 000388707600009PubMed: 28125894BACKGROUND: There have been several Radio Frequency (RF) field researches on various populations and groups of different ages in recent years. However, the most important group for research has been declared as the pregnant women and their babies. OBJECTIVE: The aim of the study was to analyse the effect on apoptotic factors of RF fields on newborn rabbit liver tissues. MATERIALS AND METHODS: Cytochrome c and AIF (Apoptosis Inducing Factor) levels were measured by western blot and caspase 1, 3 and 9 activities were measured by colorimetric method. RESULTS: Cytochrome c and AIF levels were not altered, but all caspase activities were increased in female infant rabbits that exposed to 1800 MHz GSM-like RF signals when they reached 1 month of age and caspase 1 and caspase 3 levels were decreased in male infant rabbits that exposed to 1800 MHz GSM-like RF signals between 15th and 22nd days of the gestational period. Results showed that 1800 MHz GSM-like RF exposure might lead to apoptosis in infant rabbit's liver tissues. CONCLUSION: According to the results, we suggest that postnatal RF exposure causes caspase dependent apoptosis in female infant rabbits liver tissues (Tab. 1, Fig. 2, Ref. 27). Text in PDF www.elis.sk

Piperlongumine inhibits cell growth and triggers apoptosis via intrinsic pathway in prostate cancer cells

European Cancer Congress -- 2015 -- Vienna, AUSTRIAMeral, Ogunc/0000-0001-8813-4991WOS: 000361887402220

Capsaicin inhibits cell proliferation by cytochrome c release in gastric cancer cells

PEKCAN, MERT/0000-0003-3084-125X; KOSOVA, FUNDA/0000-0001-8070-5067WOS: 000339736300042PubMed: 24682934Capsaicin (trans-8-methyl-N-vanillyl-6-nonenamide) is the principal pungent component in hot peppers. The role of capsaicin in carcinogenesis is quite controversial. Although some investigators suspect that capsaicin is a carcinogen, co-carcinogen, or tumor promoter, others have reported that it has chemopreventive and chemotherapeutic effects. The present study aimed to evaluate the cytotoxicity and chemosensitizing activities of capsaicin alone and on 5-flourouracil (5-FU)-treated gastric cancer cells. In this study, the gastric cancer cell line HGC-27 was used and capsaicin used as a chemosensitizer and 5-flourouracil (5-FU) was used as chemotherapeutic. Cytotoxicity and chemosensitizing activities were analyzed with MTT assay; supernatant levels of LDH and glucose were detected as biochemical markers of cell viability; cytochrome c and AIF were evaluated with western blot; and additionally, wound-healing assays were employed. Results suggested that capsaicin had significant anticancer abilities; such capsaicin were capable of causing multifold decreases in the half maximal inhibitory concentration IC50 value of 5-FU. The continuing controversy surrounding consumption or topical application of capsaicin clearly suggests that more well-controlled epidemiologic studies are needed to evaluate the safety and efficacy of capsaicin use. In summary, the present study demonstrated that capsaicin has the potential to be used for treating gastric carcinoma with 5-FU in vitro