Cancer-type-specific crosstalk between autophagy, necroptosis and apoptosis as a pharmacological target

Radogna, Flavia; Dicato, Mario; Diederich, Marc

doi:10.1016/j.bcp.2014.12.018

Cited by 160 publications

(156 citation statements)

References 140 publications

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“…Therefore, inhibiting autophagy in latestage cancers can suppress tumor progression by blocking this prosurvival mechanism in nutrientdeprived tumor cells and by preventing protein recycling and cellular growth [120] . On the other hand, inhibition of autophagy can also lead to a decrease in the antitumorigenic activity achieved by promoting nonapoptotic cell death.…”

Section: Autophagy Drugs In Crcmentioning

confidence: 99%

“…Future research aimed at exploring the context specific role of autophagy in particular cancer types can provide new opportunities to develop personalized thera peutic strategies based on the regulation of autophagy, and autophagy modulators may become a targetable option for enhancing the efficacy of anticancer therapies used alone or, more likely, in combination with other chemotherapeutic drugs [120] .…”

Section: Autophagy Drugs In Crcmentioning

confidence: 99%

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Autophagy in colorectal cancer: An important switch from physiology to pathology

Burada

Nicoli

Ciurea

et al. 2015

WJGO

133

131

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Colorectal cancer (CRC) remains a leading cause of cancer death in both men and women worldwide. Among the factors and mechanisms that are involved in the multifactorial etiology of CRC, autophagy is an important transformational switch that occurs when a cell shifts from normal to malignant. In recent years, multiple hypotheses have been considered regarding the autophagy mechanisms that are involved in cancer. The currently accepted hypothesis is that autophagy has dual and contradictory roles in carcinogenesis, but the precise mechanisms leading to autophagy in cancer are not yet fully defined and seem to be context dependent. Autophagy is a surveillance mechanism used by normal cells that protects them from the transformation to malignancy by removing damaged organelles and aggregated proteins and by reducing reactive oxygen species, mitochondrial abnormalities and DNA damage. However, autophagy also supports tumor formation by promoting access to nutrients that are critical to the metabolism and growth of tumor cells and by inhibiting cellular death and increasing drug resistance. Autophagy studies in CRC have focused on several molecules, mainly microtubule-associated protein 1 light chain 3, beclin 1, and autophagy related 5, with conflicting results. Beneficial effects were observed for some agents that modulate autophagy in CRC either alone or, more often, in combination with other agents. More extensive studies are needed in the future to clarify the roles of Core tip: This review describes the role of autophagy in cancer, focusing on the involvement of autophagy in colorectal cancer (CRC). Initially, we describe the steps and components of autophagy, and we then further highlight the dual role of autophagy in cancer, where it can potentially act as both a promoter and an inhibitor during the transformation from normal to malignant cell. In particular, we emphasize the major autophagy genes involved in CRC pathogenesis along with autophagymodulating agents and their modes of action in the context of CRC therapy. TOPIC HIGHLIGHT

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Section: Autophagy Drugs In Crcmentioning

confidence: 99%

Section: Autophagy Drugs In Crcmentioning

confidence: 99%

Autophagy in colorectal cancer: An important switch from physiology to pathology

Burada

Nicoli

Ciurea

et al. 2015

WJGO

133

131

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“…Nessa forma de autofagia, componentes citoplasmáticos são envolvidos por vesículas de dupla membrana e então disponibilizados para os lisossomos. As etapas desse processo incluem formação e expansão de uma membrana de isolamento conhecida como fagóforo (fases denominadas "nucleação" e "alongamento" da vesícula, respectivamente); em seguida as bordas dos fagóforos se fundem (etapa de "conclusão"), formando uma vesícula de dupla membrana conhecida como "autofagossomo", que então sequestra o material citoplasmático; o autofagossomo se funde com o lisossomo, originando uma estrutura chamada "autolisossomo", na qual o material capturado e a membrana interna são degradados (Radogna et al, 2015) …”

Section: Mtorunclassified

“…É regulada pela família de proteínas Bcl-2, as quais regulam a liberação do citocromo c por meio do aumento da permeabilidade da membrana mitocondrial externa. A permeabilização da membrana mitocondrial externa induz a ativação de uma cascata de caspases que culmina na ativação da capase efetora caspase 3 (Radogna et al, 2015) (Figura 2.5).…”

Section: Figura 23 -Esquema Ilustrativo Da Autofagiaunclassified

Resistência de células de carcinoma epidermóide bucal à terapia fotodinâmica mediada pelo ácido 5-aminolevulínico

Rosin¹

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A minha Orientadora, Prof a . Dr a . Luciana Corrêa, por sempre ouvir e discutir comigo todas as questões e dúvidas que surgiram durante o desenvolvimento desta tese e por ser essa pessoa tão generosa, inteligente e acessível. Admiro-a muito como pessoa e pesquisadora.Ao Prof. Dr. Moacir Novelli, que durante suas visitas ao laboratório sempre alegrava meu dia e por compartilhar comigo um pouco da sua imensa sabedoria. A Marina, a única companheira de profissão da Pós, que sempre esteve disposta a me ajudar e me ouvir, pela amizade, carinho e companheirismo. Pelos nossos cafés da manhã que sempre tornava meu dia mais leve e agradável.A Karla, pelo bom humor constante que sempre alegrava meu dia, por sempre me ouvir, me apoiar e pelos nossos cafezinhos.A Gabriela, por sempre estar ao meu lado me dando força e apoio, pelos nossos almoços diários na copa do departamento que tornavam meu dia mais alegre e por todo carinho e amizade.A Lara, pela amizade e por todo carinho e apoio. Por ser essa pessoa tão agradável e acessível por sempre estar disposta a me ourvir. Tenho a impressão de ter sido uma criança brincando à beira-mar, divertindo-me em descobrir uma pedrinha mais lisa ou uma concha mais bonita que as outras, enquanto o imenso oceano da verdade continua misterioso diante de meus olhos". Oral squamous cell carcinoma (SCC) is a malignant tumor with high morbidity and mortality rates, and it is difficult to treat. Conventional treatment for oral SCCs includes surgery and radiotherapy that may be followed by chemotherapy. Although these treatments are widely used, they are ineffective against some resistant tumors. Isaac Newton RESUMOOncologic photodynamic therapy (PDT) has been used as an adjuvant treatment for oral SCCs, especially in less invasive cases that require tumor reduction before surgical resection. However, like conventional treatments, PDT can induce the occurrence of resistant cell populations such as cutaneous carcinomas and colon and breast adenocarcinomas. The hypothesis that oral SCCs develop resistance to PDThas not yet been tested. Therefore, the aims of this study were to investigate whether oral SCCs (SCC9) develop resistance to several cycles of 5-aminolevulinic acidmediated PDT (5-ALA-PDT) and to determine whether the expression of markers associated with cell survival (NFB, Bcl-2, iNOS, mTOR, and Akt) is altered during this process. An oral SCC (SCC9) cell line was used, which was subjected to the following conditions: 1) Control: cultured without any treatment; 2) ALA: incubated with 5-ALA (1 mM for 4 h); 3) LED: treated with LED light (630 nm, 5.86 J/cm 2 , 22.5 J, 150 mW, 150 s); and 4) PDT: treated with 5-ALA-PDT (with the protocols of the ALA and LED groups combined) generating a lethal dose of 90%. Initially, only one cycle of PDT was administered, and cell viability was determined in all groups 24, 48, 72, and 120 h after irradiation. Subsequently, the DNA fragmentation detection assay (TUNEL) and immunofluorescence analysis of the expression of proteins NFB, Bcl-2, iNOS, pmTOR, ...

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“…Apoptosis is one of the major types of cell death, characterized by special cell morphology and pathways. The discovery of important interconnections between the apoptotic cell death mediators and signaling pathways has shed light on novel options in the targeted treatment of cancer [104].…”

Section: The Role Of Apoptosis In Chemotherapymentioning

confidence: 99%

Comparison of the effects of resistance modifiers on prostate cancer, mouse lymphoma and colon cancer cells

Csonka

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Cancer-type-specific crosstalk between autophagy, necroptosis and apoptosis as a pharmacological target

Cited by 160 publications

References 140 publications

Autophagy in colorectal cancer: An important switch from physiology to pathology

Autophagy in colorectal cancer: An important switch from physiology to pathology

Resistência de células de carcinoma epidermóide bucal à terapia fotodinâmica mediada pelo ácido 5-aminolevulínico

Comparison of the effects of resistance modifiers on prostate cancer, mouse lymphoma and colon cancer cells

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