human
The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
    ###
    INPUT: AIMS Cisplatin-induced nephrotoxicity is associated with increased oxidative stress and inflammatory cytokines in the kidney . Epigallocatechin-3-gallate ( EGCG ) has anti-oxidant , anti-inflammatory , and anti-tumorigenic properties . In this study , we investigated the effects of EGCG on cisplatin-induced nephrotoxicity and potential mechanisms by which it enhances antioxidant activities and resolves inflammation after EGCG treatment during cisplatin-induced nephrotoxicity . MAIN METHODS Twenty-eight rats were divided into four groups as control ( group 1 ; no treatment ; n=7 ) , EGCG ( group 2 ; n=7 ) , cisplatin ( group 3 ; n=7 ) or cisplatin and EGCG ( group 4 ; n=7 ) . After 2 days of EGCG treatment at a dose of l00 mg/kg BW , rats were treated with a single i.p. injection of cisplatin ( 7 mg/kg BW ) . On day 12 ( 10days after the cisplatin treatment ) , all rats were sacrificed by cervical dislocation . The level of protein was examined by Western blotting . KEY FINDINGS Cisplatin caused a significant decrease in the expression nuclear levels of NF-E2-related factor-2 ( Nrf2 ) , heme oxygenase-1(HO-1) , and an increase in the levels of nuclear factor-kappa B ( NF-kappaB p65 ) and 4-hydroxynonenal ( HNE ) an oxidative stress marker . EGCG supplementation significantly improved the changes associated with cisplatin nephrotoxicity by increasing levels of Nrf-2 and HO-1 , and decreasing levels of NF-kappaB and HNE . Renal activities of antioxidant enzymes ( catalase , superoxide dismutase , glutathione peroxidase ) and glutathione were significantly lower in cisplatin-treated rats compared with control rats , and EGCG treatment significantly increased the activities of antioxidant enzymes and glutathione ( P&lt;0.001 ) . SIGNIFICANCE The results suggest that Nrf2/HO-1 signaling pathway may be the primary target for prevention of cisplatin-induced nephrotoxicity by EGCG , and that reduces it inflammation by inhibiting NF-kappaB .
    OUTPUT:

agent
tumor promoting inflammation
The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
    ###
    INPUT: AIMS Cisplatin-induced nephrotoxicity is associated with increased oxidative stress and inflammatory cytokines in the kidney . Epigallocatechin-3-gallate ( EGCG ) has anti-oxidant , anti-inflammatory , and anti-tumorigenic properties . In this study , we investigated the effects of EGCG on cisplatin-induced nephrotoxicity and potential mechanisms by which it enhances antioxidant activities and resolves inflammation after EGCG treatment during cisplatin-induced nephrotoxicity . MAIN METHODS Twenty-eight rats were divided into four groups as control ( group 1 ; no treatment ; n=7 ) , EGCG ( group 2 ; n=7 ) , cisplatin ( group 3 ; n=7 ) or cisplatin and EGCG ( group 4 ; n=7 ) . After 2 days of EGCG treatment at a dose of l00 mg/kg BW , rats were treated with a single i.p. injection of cisplatin ( 7 mg/kg BW ) . On day 12 ( 10days after the cisplatin treatment ) , all rats were sacrificed by cervical dislocation . The level of protein was examined by Western blotting . KEY FINDINGS Cisplatin caused a significant decrease in the expression nuclear levels of NF-E2-related factor-2 ( Nrf2 ) , heme oxygenase-1(HO-1) , and an increase in the levels of nuclear factor-kappa B ( NF-kappaB p65 ) and 4-hydroxynonenal ( HNE ) an oxidative stress marker . EGCG supplementation significantly improved the changes associated with cisplatin nephrotoxicity by increasing levels of Nrf-2 and HO-1 , and decreasing levels of NF-kappaB and HNE . Renal activities of antioxidant enzymes ( catalase , superoxide dismutase , glutathione peroxidase ) and glutathione were significantly lower in cisplatin-treated rats compared with control rats , and EGCG treatment significantly increased the activities of antioxidant enzymes and glutathione ( P&lt;0.001 ) . SIGNIFICANCE The results suggest that Nrf2/HO-1 signaling pathway may be the primary target for prevention of cisplatin-induced nephrotoxicity by EGCG , and that reduces it inflammation by inhibiting NF-kappaB .
    OUTPUT:
