Matches in SemOpenAlex for { <https://semopenalex.org/work/W2890923034> ?p ?o ?g. }
Showing items 1 to 86 of
86
with 100 items per page.
- W2890923034 endingPage "332" @default.
- W2890923034 startingPage "321" @default.
- W2890923034 abstract "Autophagy is a quality control process executed at the basal level in almost all cell types. However, in cancer cells, autophagy is activated by several stimuli, including hypoxia. Depending on tumor type, stage, and genetic context, autophagy is a double-edged sword. Autophagy promotes regression in newly established tumors; however, it supports tumor progression in well-established tumors by maintaining cancer cell survival under stress conditions. These data, in addition to the emerging role of autophagy in impairing antitumor immunity, have attracted significant interest in developing autophagy inhibitors as a new approach to cancer treatment. The enthusiasm for developing selective drugs inhibiting autophagy has been seriously challenged by the discovery that most autophagy-related proteins display nonautophagic functions. Autophagy inhibitors chloroquine and hydroxychloroquine are currently being investigated in several clinical trials in combination with standard anticancer therapies. Here, we provide a brief overview on the nonautophagic function of autophagy-related proteins and summarize the major mechanisms whereby autophagy modulation could positively or negatively impact cancer therapies. We also focus on the emerging role of targeting autophagy in the improvement of NK-mediated antitumor immunity through the regulation of CCL5 and its receptors' expression in melanoma, and we provide some clues revealing how autophagy modulators could be exploited to improve cancer immunotherapies." @default.
- W2890923034 created "2018-09-27" @default.
- W2890923034 creator A5003314533 @default.
- W2890923034 creator A5010992631 @default.
- W2890923034 creator A5015331828 @default.
- W2890923034 creator A5022850024 @default.
- W2890923034 creator A5024581567 @default.
- W2890923034 creator A5042997291 @default.
- W2890923034 creator A5052327708 @default.
- W2890923034 creator A5069638247 @default.
- W2890923034 creator A5091343254 @default.
- W2890923034 date "2018-01-01" @default.
- W2890923034 modified "2023-09-27" @default.
- W2890923034 title "Driving Cytotoxic Natural Killer Cells into Melanoma: If CCL5 Plays the Music, Autophagy Calls the Shots" @default.
- W2890923034 doi "https://doi.org/10.1615/critrevoncog.2018027526" @default.
- W2890923034 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30311563" @default.
- W2890923034 hasPublicationYear "2018" @default.
- W2890923034 type Work @default.
- W2890923034 sameAs 2890923034 @default.
- W2890923034 citedByCount "5" @default.
- W2890923034 countsByYear W28909230342020 @default.
- W2890923034 countsByYear W28909230342021 @default.
- W2890923034 countsByYear W28909230342022 @default.
- W2890923034 countsByYear W28909230342023 @default.
- W2890923034 crossrefType "journal-article" @default.
- W2890923034 hasAuthorship W2890923034A5003314533 @default.
- W2890923034 hasAuthorship W2890923034A5010992631 @default.
- W2890923034 hasAuthorship W2890923034A5015331828 @default.
- W2890923034 hasAuthorship W2890923034A5022850024 @default.
- W2890923034 hasAuthorship W2890923034A5024581567 @default.
- W2890923034 hasAuthorship W2890923034A5042997291 @default.
- W2890923034 hasAuthorship W2890923034A5052327708 @default.
- W2890923034 hasAuthorship W2890923034A5069638247 @default.
- W2890923034 hasAuthorship W2890923034A5091343254 @default.
- W2890923034 hasConcept C121608353 @default.
- W2890923034 hasConcept C151730666 @default.
- W2890923034 hasConcept C190283241 @default.
- W2890923034 hasConcept C203014093 @default.
- W2890923034 hasConcept C203522944 @default.
- W2890923034 hasConcept C2776107976 @default.
- W2890923034 hasConcept C2779343474 @default.
- W2890923034 hasConcept C502942594 @default.
- W2890923034 hasConcept C54355233 @default.
- W2890923034 hasConcept C55493867 @default.
- W2890923034 hasConcept C71924100 @default.
- W2890923034 hasConcept C86803240 @default.
- W2890923034 hasConcept C8891405 @default.
- W2890923034 hasConcept C95444343 @default.
- W2890923034 hasConcept C96232424 @default.
- W2890923034 hasConceptScore W2890923034C121608353 @default.
- W2890923034 hasConceptScore W2890923034C151730666 @default.
- W2890923034 hasConceptScore W2890923034C190283241 @default.
- W2890923034 hasConceptScore W2890923034C203014093 @default.
- W2890923034 hasConceptScore W2890923034C203522944 @default.
- W2890923034 hasConceptScore W2890923034C2776107976 @default.
- W2890923034 hasConceptScore W2890923034C2779343474 @default.
- W2890923034 hasConceptScore W2890923034C502942594 @default.
- W2890923034 hasConceptScore W2890923034C54355233 @default.
- W2890923034 hasConceptScore W2890923034C55493867 @default.
- W2890923034 hasConceptScore W2890923034C71924100 @default.
- W2890923034 hasConceptScore W2890923034C86803240 @default.
- W2890923034 hasConceptScore W2890923034C8891405 @default.
- W2890923034 hasConceptScore W2890923034C95444343 @default.
- W2890923034 hasConceptScore W2890923034C96232424 @default.
- W2890923034 hasIssue "5-6" @default.
- W2890923034 hasLocation W28909230341 @default.
- W2890923034 hasLocation W28909230342 @default.
- W2890923034 hasOpenAccess W2890923034 @default.
- W2890923034 hasPrimaryLocation W28909230341 @default.
- W2890923034 hasRelatedWork W2070958946 @default.
- W2890923034 hasRelatedWork W2086604883 @default.
- W2890923034 hasRelatedWork W2135512477 @default.
- W2890923034 hasRelatedWork W2505176208 @default.
- W2890923034 hasRelatedWork W2512384325 @default.
- W2890923034 hasRelatedWork W2555159264 @default.
- W2890923034 hasRelatedWork W2771066073 @default.
- W2890923034 hasRelatedWork W2809831584 @default.
- W2890923034 hasRelatedWork W3112751811 @default.
- W2890923034 hasRelatedWork W3206598336 @default.
- W2890923034 hasVolume "23" @default.
- W2890923034 isParatext "false" @default.
- W2890923034 isRetracted "false" @default.
- W2890923034 magId "2890923034" @default.
- W2890923034 workType "article" @default.