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    Capsaicin inhibits cell proliferation by cytochrome c release in gastric cancer cells
    (Sage Publications Ltd, 2014) Meral, Ogunc; Alpay, Merve; Kismali, Gorkem; Kosova, Funda; Cakir, Dilek Ulker; Pekcan, Mert; Yigit, Serbulent
    Capsaicin (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.
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    Capsaicin inhibits proliferation and chemosensitizes gastric carcinoma cells to 5-Fluorouracil
    (Amer Assoc Cancer Research, 2014) Kismali, Gorkem; Alpay, Merve; Meral, Ogunc; Kosova, Funda; Cakir, Dilek Ulker; Sel, Tevhide
    [Anstract Not Available]
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    Oxidative status of colitis-associated cancer model induced by azoxymethane /dextran sulfate sodium and the effects of COX-2 inhibitor in mice
    (Ankara Univ Press, 2019) Kismali, Gorkem; Uner, Aykut Gokturk; Meral, Ogunc; Alpay, Merve; Salmanoglu, Berrin; Ulker Cakir, Dilek; Kosova, Funda
    Natural products and anti-inflammatory agents including cyclooxygenase-2 (COX-2) inhibitors which is a type of nonsteroidal anti-inflammatory drugs (NSAIDs) are highly considerable interest for the prevention of carcinogenesis. The objective of this study is to evaluate the oxidative status of colitis-associated cancer induced by azoxymethane (AOM)/dextran sulfate sodium (DSS), and the effects of COX-2 inhibitor in mice. Totally 40 mice were randomized and divided to four groups. All animals except control and Cox-2 inhibitor alone group received AOM/DSS to establish colitis-associated cancer model as reported elsewhere. COX-2 preferential inhibitor meloxicam was used to minimize side effects such as gastrointestinal hemorrhage. Meloxicam were used (5mg/kg, intraperitoneal) three times a week with meloxicam alone and AOM/DSS + meloxicam group. Superoxide dismutase (SOD), Glutathione peroxidase (GPx), Malondialdehyde (MDA) and Advanced Oxidation Protein Products (AOPP) which all of them are oxidative stress markers were measured by spectrophotometrically. The combination treatment of Meloxicam and AOM/DSS significantly increased (P<0.05) SOD activities in mice. GPx activities were found significantly increased (P<0.05) in Meloxicam and AOM/DSS combinations or alone. There were no differences between the control and treatment groups of MDA levels. AOPP levels of Meloxicam and AOM/DSS combination group were found higher than the other groups. Meloxicam and /or AOM/DSS treatment not caused lipid peroxidations, but increased the antioxidant enzymes and Advanced Oxidation Protein Products levels.
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    Piperlongumine inhibits cell growth and enhances TRAIL-induced apoptosis in prostate cancer cells
    (Wolters Kluwer Medknow Publications, 2020) Kismali, Gorkem; Ceylan, Ahmet; Meral, Ogunc; Alpay, Merve; Kosova, Funda; Cakir, Dilek Ulker; Yurdakok-Dikmen, Begum
    Objective: To investigate whether piperlongumine can sensitize prostate cancer cells to tumor necrosis factor-related apoptosis- inducing ligand (TRAIL) and trigger apoptosis in prostate cells. Methods: Human prostate cancer cell lines PC3, LNCaP, and VCaP were cultured with piperlongumine and TRAIL. Then, cell proliferation, migration, caspase activation, apoptotic protein expressions, and death receptor expressions were measured. Results: Piperlongumine inhibited cell proliferation at low doses (<10 mu M) alone and in combination with TRAIL (25 ng/mL), induced apoptosis, and suppressed cyclooxygenase activation. Additionally, piperlongumine induced expression of death receptors which potentiated TRAIL-induced apoptosis in cancer cells but did not affect decoy receptors. Piperlongumine also downregulated tumor cell-survival pathways, inhibited colony formation and migration of cancer cells alone or in combination with TRAIL. The combination of piperlongumine with TRAIL was found to be synergistic. Conclusions: Our findings indicate that piperlongumine can sensitize cancer cells to TRAIL through the upregulation of death receptors and can trigger apoptosis with the downregulation of anti- apoptotic proteins.