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.
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    INPUT: Sunitinib is an oral multitargeted receptor tyrosine kinase inhibitor with antiangiogenic and antitumor activity that mainly targets vascular endothelial growth factor receptors , and recently , it has been shown to be an active agent for the treatment of malignant pheochromocytomas . Previously , we demonstrated that sunitinib directly inhibited mTORC1 signaling in rat pheochromocytoma PC12 cells . Although autophagy is a highly regulated cellular process , its relevance to cancer seems to be complicated . It is of note that inhibition of mTORC1 is a prerequisite for autophagy induction . Indeed , direct mTORC1 inhibition initiates ULK1/2 autophosphorylation and subsequent Atg13 and FIP200 phosphorylation , inducing autophagy . Here , we demonstrated that sunitinib significantly increased the levels of LC3-II , concomitant with a decrease of p62 in PC12 cells . Following sunitinib treatment , immunofluorescent imaging revealed a marked increased punctate LC3-II distribution . Furthermore , Atg13 knockdown significantly reduced its protein level , which in turn abolished sunitinib-induced autophagy . Moreover , inhibition of autophagy by siRNAs targeting Atg13 or by pharmacological inhibition with ammonium chloride , enhanced both sunitinib-induced apoptosis and anti-proliferation . Thus , sunitinib-induced autophagy is dependent on the suppression of mTORC1 signaling and the formation of ULK1/2-Atg13-FIP200 complexes . Inhibition of autophagy may be a promising therapeutic option for improving the anti-tumor effect of sunitinib .
    OUTPUT:

agent
resisting cell death
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: Sunitinib is an oral multitargeted receptor tyrosine kinase inhibitor with antiangiogenic and antitumor activity that mainly targets vascular endothelial growth factor receptors , and recently , it has been shown to be an active agent for the treatment of malignant pheochromocytomas . Previously , we demonstrated that sunitinib directly inhibited mTORC1 signaling in rat pheochromocytoma PC12 cells . Although autophagy is a highly regulated cellular process , its relevance to cancer seems to be complicated . It is of note that inhibition of mTORC1 is a prerequisite for autophagy induction . Indeed , direct mTORC1 inhibition initiates ULK1/2 autophosphorylation and subsequent Atg13 and FIP200 phosphorylation , inducing autophagy . Here , we demonstrated that sunitinib significantly increased the levels of LC3-II , concomitant with a decrease of p62 in PC12 cells . Following sunitinib treatment , immunofluorescent imaging revealed a marked increased punctate LC3-II distribution . Furthermore , Atg13 knockdown significantly reduced its protein level , which in turn abolished sunitinib-induced autophagy . Moreover , inhibition of autophagy by siRNAs targeting Atg13 or by pharmacological inhibition with ammonium chloride , enhanced both sunitinib-induced apoptosis and anti-proliferation . Thus , sunitinib-induced autophagy is dependent on the suppression of mTORC1 signaling and the formation of ULK1/2-Atg13-FIP200 complexes . Inhibition of autophagy may be a promising therapeutic option for improving the anti-tumor effect of sunitinib .
    OUTPUT:
