PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 26812869-0 2015 The effect of nicotine on the expressions of the alpha7 nicotinic receptor gene and Bax and Bcl-2 proteins in the mammary gland epithelial-7 breast cancer cell line and its relationship to drug resistance. Nicotine 14-22 BCL2 apoptosis regulator Homo sapiens 92-97 26812869-4 2015 This study focuses on the effect of nicotine on the expressions of the alpha7 nicotinic receptor gene and Bax and Bcl-2 proteins in mammary gland epithelial-7 (MCF-7) breast cancer cells and its relationship to drug resistance. Nicotine 36-44 BCL2 apoptosis regulator Homo sapiens 114-119 25151121-0 2014 Nicotine mediates oxidative stress and apoptosis through cross talk between NOX1 and Bcl-2 in lung epithelial cells. Nicotine 0-8 BCL2 apoptosis regulator Homo sapiens 85-90 25151121-8 2014 Overexpression of Bcl-2 completely prevented nicotine"s detrimental effects, suggesting Bcl-2as a downstream key regulator in nicotine/NOX1-induced cell damage. Nicotine 45-53 BCL2 apoptosis regulator Homo sapiens 18-23 25151121-8 2014 Overexpression of Bcl-2 completely prevented nicotine"s detrimental effects, suggesting Bcl-2as a downstream key regulator in nicotine/NOX1-induced cell damage. Nicotine 45-53 BCL2 apoptosis regulator Homo sapiens 88-93 25151121-8 2014 Overexpression of Bcl-2 completely prevented nicotine"s detrimental effects, suggesting Bcl-2as a downstream key regulator in nicotine/NOX1-induced cell damage. Nicotine 126-134 BCL2 apoptosis regulator Homo sapiens 18-23 25151121-8 2014 Overexpression of Bcl-2 completely prevented nicotine"s detrimental effects, suggesting Bcl-2as a downstream key regulator in nicotine/NOX1-induced cell damage. Nicotine 126-134 BCL2 apoptosis regulator Homo sapiens 88-93 24548862-0 2014 Nicotine increases the resistance of lung cancer cells to cisplatin through enhancing Bcl-2 stability. Nicotine 0-8 BCL2 apoptosis regulator Homo sapiens 86-91 24548862-3 2014 METHODS: In this study, we used immunoblotting and immunoprecipitation methods to test the ubiquitination and degradation of Bcl-2 affected by nicotine in lung cancer cells. Nicotine 143-151 BCL2 apoptosis regulator Homo sapiens 125-130 24548862-5 2014 RESULTS: We demonstrated that the addition of nicotine greatly attenuated Bcl-2 ubiquitination and degradation, which further desensitised lung cancer cells to cisplatin-induced cytotoxicity. Nicotine 46-54 BCL2 apoptosis regulator Homo sapiens 74-79 24548862-6 2014 In this process, Bcl-2 was persistently phosphorylated in the cells cotreated with nicotine and cisplatin. Nicotine 83-91 BCL2 apoptosis regulator Homo sapiens 17-22 24548862-7 2014 Furthermore, Akt was proven to be responsible for sustained activation of Bcl-2 by nicotine, which further antagonised cisplatin-mediated apoptotic signalling. Nicotine 83-91 BCL2 apoptosis regulator Homo sapiens 74-79 24548862-8 2014 CONCLUSIONS: Our study suggested that nicotine activates its downstream signalling to interfere with the ubiquitination process and prevent Bcl-2 from being degraded in lung cancer cells, resulting in the increase of chemoresistance. Nicotine 38-46 BCL2 apoptosis regulator Homo sapiens 140-145 22187147-7 2012 Interestingly, most of the differentially expressed genes in these pathways leading to nuclear factor kappaB (NF-kappaB) activation and those important inhibitors of pathways leading to apoptosis, including FLIP and Bcl-2, were up-regulated by nicotine. Nicotine 244-252 BCL2 apoptosis regulator Homo sapiens 216-221 24967145-0 2014 Bcl2 Family Functions as Signaling Target in Nicotine-/NNK-Induced Survival of Human Lung Cancer Cells. Nicotine 45-53 BCL2 apoptosis regulator Homo sapiens 0-4 24967145-7 2014 In the past several years, multiple signaling links between nicotine/NNK and Bcl2 family members have been identified that regulate survival and proliferation. Nicotine 60-68 BCL2 apoptosis regulator Homo sapiens 77-81 12421819-6 2003 Nicotine induces activation of PKC alpha and the MAPKs ERK1 and ERK2, which are physiological Bcl2 kinases. Nicotine 0-8 BCL2 apoptosis regulator Homo sapiens 94-98 16144975-9 2005 In contrast, the bcl-2 antagonist ethyl[2-amino-6-bromo-4-(1-cyano-2-ethoxy-2-oxoethyl)]-4H-chromene-3-carboxylate (HA 14-1) reversed the protective effects of the three AChE inhibitors and that of nicotine. Nicotine 198-206 BCL2 apoptosis regulator Homo sapiens 17-22 22382680-9 2012 Under various doses of nicotine, a decrease in the anti-apoptotic protein Bcl-2, but an increase in p53 and cleaved caspase-3 protein levels, was detected in a dose-dependent manner. Nicotine 23-31 BCL2 apoptosis regulator Homo sapiens 74-79 20727180-4 2010 RESULTS: While low concentrations of nicotine induced activation of NF-kappaB, Akt, Bcl2, MAPKs, AP1 and IAPs in H1299, it failed to induce NF-kappaB in A549, and compared to H1299, almost 100 times higher concentration of nicotine was required to induce all other survival signals in A549. Nicotine 37-45 BCL2 apoptosis regulator Homo sapiens 84-88 20339300-8 2010 Real-time PCR indicated that the expression of Bcl-2, Pax3, Bmp4 and Slug was down-regulated in the nicotine group, while the expression of P53, Bax and Msx1 was up-regulated. Nicotine 100-108 BCL2 apoptosis regulator Homo sapiens 47-52 12421819-0 2003 A functional role for nicotine in Bcl2 phosphorylation and suppression of apoptosis. Nicotine 22-30 BCL2 apoptosis regulator Homo sapiens 34-38 12421819-4 2003 It is possible that nicotine may regulate Bcl2 to stimulate cell survival. Nicotine 20-28 BCL2 apoptosis regulator Homo sapiens 42-46 12421819-5 2003 Here we report that nicotine can induce Bcl2 phosphorylation exclusively at the serine 70 site in association with prolonged survival of SCLC H82 cells expressing wild-type but not the phosphorylation-deficient S70A mutant Bcl2 after treatment with chemotherapeutic agents (i.e. cisplatin or VP-16). Nicotine 20-28 BCL2 apoptosis regulator Homo sapiens 40-44 12421819-5 2003 Here we report that nicotine can induce Bcl2 phosphorylation exclusively at the serine 70 site in association with prolonged survival of SCLC H82 cells expressing wild-type but not the phosphorylation-deficient S70A mutant Bcl2 after treatment with chemotherapeutic agents (i.e. cisplatin or VP-16). Nicotine 20-28 BCL2 apoptosis regulator Homo sapiens 223-227 12421819-7 2003 Furthermore, ET-18-OCH3, a specific phospholipase C (PLC) inhibitor, blocks nicotine-stimulated Bcl2 phosphorylation and promotes apoptosis, suggesting that PLC may be involved in nicotine activation of Bcl2 kinases. Nicotine 76-84 BCL2 apoptosis regulator Homo sapiens 96-100 12421819-7 2003 Furthermore, ET-18-OCH3, a specific phospholipase C (PLC) inhibitor, blocks nicotine-stimulated Bcl2 phosphorylation and promotes apoptosis, suggesting that PLC may be involved in nicotine activation of Bcl2 kinases. Nicotine 76-84 BCL2 apoptosis regulator Homo sapiens 203-207 12421819-7 2003 Furthermore, ET-18-OCH3, a specific phospholipase C (PLC) inhibitor, blocks nicotine-stimulated Bcl2 phosphorylation and promotes apoptosis, suggesting that PLC may be involved in nicotine activation of Bcl2 kinases. Nicotine 180-188 BCL2 apoptosis regulator Homo sapiens 96-100 12421819-7 2003 Furthermore, ET-18-OCH3, a specific phospholipase C (PLC) inhibitor, blocks nicotine-stimulated Bcl2 phosphorylation and promotes apoptosis, suggesting that PLC may be involved in nicotine activation of Bcl2 kinases. Nicotine 180-188 BCL2 apoptosis regulator Homo sapiens 203-207 12421819-9 2003 Thus, nicotine-induced cell survival results, at least in part, from a mechanism that involves Bcl2 phosphorylation. Nicotine 6-14 BCL2 apoptosis regulator Homo sapiens 95-99 12421819-10 2003 Therefore, novel therapeutic strategies for lung cancer in which Bcl2 is expressed may be used to abrogate the anti-apoptotic activity of Bcl2 by inhibiting multiple upstream nicotine-activated pathways. Nicotine 175-183 BCL2 apoptosis regulator Homo sapiens 65-69 12421819-10 2003 Therefore, novel therapeutic strategies for lung cancer in which Bcl2 is expressed may be used to abrogate the anti-apoptotic activity of Bcl2 by inhibiting multiple upstream nicotine-activated pathways. Nicotine 175-183 BCL2 apoptosis regulator Homo sapiens 138-142 33010382-9 2020 Furthermore, 3MA reversed both the nicotine-induced decrease in Bcl-2 and the increase in Bax in both groups. Nicotine 35-43 BCL2 apoptosis regulator Homo sapiens 64-69 9600337-2 1998 The present study provides evidence that nicotine (a) activates the mitogen-activated protein (MAP) kinase signalling pathway in lung cancer cells, specifically extracellular signal-regulated kinase (ERK2), resulting in increased expression of the bcl-2 protein and inhibition of apoptosis in these cells; and (b) blocks the inhibition of protein kinase C (PKC) and ERK2 activity in lung cancer cells by anti-cancer agents, such as therapeutic opioid drugs, and thus can adversely affect cancer therapy. Nicotine 41-49 BCL2 apoptosis regulator Homo sapiens 248-253 33884179-10 2021 Although nicotine at concentrations up to 10 muM did not cause cell death, treatment of HCAEC with 10 nM nicotine in the presence of 13.8 mM dextrose aggravated ER stress, increased cell death, increased cleaved caspase 3 and BID, and decreased BCL2. Nicotine 105-113 BCL2 apoptosis regulator Homo sapiens 245-249 11278378-4 2001 Levels of phosphorylated Akt, an effector of PI3K, and Bcl-2 were increased by nicotine. Nicotine 79-87 BCL2 apoptosis regulator Homo sapiens 55-60 27028622-10 2016 Nicotine increased the Bax/Bcl-2 ratio, which was attenuated by N-acetyl-L-cysteine, the NF-kappaB inhibitor, Bay 11-7082, and hexamethonium, a non-specific nAChR blocker. Nicotine 0-8 BCL2 apoptosis regulator Homo sapiens 27-32 31935534-8 2020 Co-treatment of cisplatin and nicotine attenuated the effect of cisplatin on Bcl-2 expression. Nicotine 30-38 BCL2 apoptosis regulator Homo sapiens 77-82 31935534-9 2020 In addition, the effect of nicotine on cell survival under cisplatin treatment was attenuated with the addition of the Bcl-2 inhibitor ABT-737. Nicotine 27-35 BCL2 apoptosis regulator Homo sapiens 119-124 33927788-3 2020 Epidemiological studies have shown that nicotine consumption decreases PD prevalence through neuroprotective mechanisms activation associated with the overstimulation of signaling pathways (SP) such as PI3K/AKT through nicotinic acetylcholine receptors (e.g alpha7 nAChRs) and over-expression of anti-apoptotic genes such as Bcl-2. Nicotine 40-48 BCL2 apoptosis regulator Homo sapiens 325-330 33927788-9 2020 Results: Our model was able to predict the potential neuroprotective activity of seven new nicotine analogs based on the binomial Bcl-2 response regulated by the activation of PI3K/AKT. Nicotine 91-99 BCL2 apoptosis regulator Homo sapiens 130-135 29972271-7 2018 Simultaneously, nicotine induces pancreatic islet cell apoptosis by modulating DeltaPsim via increased cytosolic Ca2+ level, altered Bcl-2, Bax, cytochrome c, caspase-9, PARP expressions which were prevented by the supplementation of folic acid and vitamin B12 . Nicotine 16-24 BCL2 apoptosis regulator Homo sapiens 133-138 26909550-12 2016 This effect correlated with the induction of Bcl-2, Bax, Survivin and Caspase-3 by nicotine in gastric cell lines. Nicotine 83-91 BCL2 apoptosis regulator Homo sapiens 45-50