{"doi":"10.1155/2013/102735","title":"Role of the Crosstalk between Autophagy and Apoptosis in Cancer","abstract":"<jats:p>Autophagy and apoptosis are catabolic pathways essential for organismal homeostasis. Autophagy is normally a cell-survival pathway involving the degradation and recycling of obsolete, damaged, or harmful macromolecular assemblies; however, excess autophagy has been implicated in type II cell death. Apoptosis is the canonical programmed cell death pathway. Autophagy and apoptosis have now been shown to be interconnected by several molecular nodes of crosstalk, enabling the coordinate regulation of degradation by these pathways. Normally, autophagy and apoptosis are both tumor suppressor pathways. Autophagy fulfils this role as it facilitates the degradation of oncogenic molecules, preventing development of cancers, while apoptosis prevents the survival of cancer cells. Consequently, defective or inadequate levels of either autophagy or apoptosis can lead to cancer. However, autophagy appears to have a dual role in cancer, as it has now been shown that autophagy also facilitates the survival of tumor cells in stress conditions such as hypoxic or low-nutrition environments. Here we review the multiple molecular mechanisms of coordination of autophagy and apoptosis and the role of the proteins involved in this crosstalk in cancer. A comprehensive understanding of the interconnectivity of autophagy and apoptosis is essential for the development of effective cancer therapeutics.</jats:p>","journal":"Journal of Oncology","year":2013,"id":18996,"datarank":10.813219692144575,"base_score":5.717027701406222,"endowment":5.717027701406222,"self_citation_contribution":0.8575541552109334,"citation_network_contribution":9.95566553693364,"self_endowment_contribution":0.8575541552109334,"citer_contribution":9.95566553693364,"corpus_percentile":null,"corpus_rank":null,"citation_count":303,"citer_count":200,"citers_with_citation_signal":200,"citers_with_endowment":200,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":null,"is_oa":false,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":130036,"name":"Yang Mei","orcid":null,"position":1,"is_corresponding":false},{"id":130037,"name":"Sangita Sinha","orcid":null,"position":2,"is_corresponding":false},{"id":130035,"name":"Minfei Su","orcid":null,"position":0,"is_corresponding":false}],"reference_count":0,"raw_metadata":{"has_enrichment":true,"base_score":5.717027701406222,"endowment":5.717027701406222,"datacite_reuse_total":0,"file_count":0,"downloads":0,"views":0,"has_version_chain":false,"is_dataset":false,"is_oa":false,"pmid":"23840208","pmcid":"PMC3687500","openalex_id":"https://openalex.org/W2159372512","authors":[],"funders":[{"funder_name":"National Institutes of Health","grant_id":"R21 AI078198","title":null},{"funder_name":"National Institutes of Health","grant_id":"P30 GM103332-01","title":null},{"funder_name":"National Institutes of Health","grant_id":"HRD-0811239","title":null},{"funder_name":"NIAID NIH HHS","grant_id":"R21 AI078108","title":null},{"funder_name":"NIGMS NIH HHS","grant_id":"P30 GM103332","title":null},{"funder_name":"National Science Foundation","grant_id":"0811239","title":"ADVANCE Institutional Transformation Award: NDSU ADVANCE FORWARD - Transforming a Gendered Institution"},{"funder_name":"National Institutes of Health","grant_id":"5P30GM103332-03","title":"Pilot Projects: Core D"}],"total_grants":7,"fwci":14.4728,"citation_percentile":0.99347081,"influential_citations":6,"citation_trend":[{"year":2013,"count":3},{"year":2014,"count":24},{"year":2015,"count":20},{"year":2016,"count":24},{"year":2017,"count":13},{"year":2018,"count":20},{"year":2019,"count":15},{"year":2020,"count":30},{"year":2021,"count":34},{"year":2022,"count":50},{"year":2023,"count":20},{"year":2024,"count":28},{"year":2025,"count":21},{"year":2026,"count":1}],"oa_status":"hybrid","license":"cc-by","oa_locations":[{"url":"https://downloads.hindawi.com/journals/jo/2013/102735.pdf","host_type":"journal"},{"url":"https://downloads.hindawi.com/journals/jo/2013/102735.pdf","host_type":"GOLD"},{"url":"https://downloads.hindawi.com/journals/jo/2013/102735.pdf","host_type":"publisher"},{"url":"http://downloads.hindawi.com/journals/jo/2013/102735.pdf","host_type":"publisher"},{"url":"http://downloads.hindawi.com/journals/jo/2013/102735.xml","host_type":"publisher"},{"url":"https://doi.org/10.1155/2013/102735","host_type":"journal"},{"url":"https://pubmed.ncbi.nlm.nih.gov/23840208","host_type":"repository"},{"url":"https://doaj.org/article/8c928581e5874be6bd95bae3faaf79d4","host_type":"repository"},{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/3687500","host_type":"repository"},{"url":"https://europepmc.org/articles/PMC3687500","host_type":"Europe_PMC"},{"url":"https://europepmc.org/articles/PMC3687500?pdf=render","host_type":"Europe_PMC"},{"url":"http://dx.doi.org/10.1155/2013/102735","host_type":""},{"url":"https://dx.doi.org/10.1155/2013/102735","host_type":""}],"fields_of_study":["Autophagy in Disease and Therapy","Endoplasmic Reticulum Stress and Disease","Studies on Chitinases and Chitosanases","Biology","Medicine","0301 basic medicine","0303 health sciences","03 medical and health sciences"],"mesh_terms":[],"keywords":["Autophagy","Crosstalk","Apoptosis","Cell biology","Programmed cell death","Cancer cell","Suppressor","Cancer research","Biology","Cancer","Biochemistry","Genetics","Review Article"],"sdg_mappings":[{"sdg_number":3,"sdg_label":"3. 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