Uncoordinated 51‐like kinase 2 signaling pathway regulates epithelial‐mesenchymal transition in A549 lung cancer cells

Kim, Young Hwan; Baek, Seung Hoon; Kim, Eun Kyoung; Ha, Jung Min; Jin, Seo Yeon; Lee, Hye Sun; Ha, Hong Koo; Song, Sang Heon; Kim, Sun Ja; Shin, Hwa Kyoung; Yong, Jeongsik; Kim, Do-Hyung; Kim, Chi Dae; Bae, Sun Sik

doi:10.1002/1873-3468.12172

Cited by 34 publications

(23 citation statements)

References 41 publications

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“…One study reported that autophagy is required for TGF-β induced EMT and invasion of hepatocellular carcinoma cell lines, in part through a dependence on autophagy for TGF-β signaling (53). It was also shown that Unc51-like Autophagy Activating Kinase-2 (ULK2), which promotes autophagy through phosphorylation of the Beclin1-containing initiation complex, stimulates EMT, downregulation of E-cadherin and increased invasiveness in vitro (54). Increased autophagy was also linked to a more mesenchymal stem-like phenotype and to be required for invasion and migration of glioblastoma stem cell lines (43) although a more recent study has argued that autophagy limits glioblastoma tumor cell migration through down-regulation of Snail and Slug (55).…”

Section: Links Between Autophagy Epithelial-mesenchymal Transition Amentioning

confidence: 99%

Autophagy in cancer metastasis

2016

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Autophagy is a highly conserved self-degradative process that plays a key role in cellular stress responses and survival. Recent work has begun to explore the function of autophagy in cancer metastasis, which is of particular interest given the dearth of effective therapeutic options for metastatic disease. Autophagy is induced upon progression of various human cancers to metastasis and together with data from genetically engineered mice and experimental metastasis models, a role for autophagy at nearly every phase of the metastatic cascade has been identified. Specifically, autophagy has been shown to be involved in modulating tumor cell motility and invasion, cancer stem cell viability and differentiation, resistance to anoikis, epithelial-to-mesenchymal transition, tumor cell dormancy and escape from immune surveillance, with emerging functions in establishing the pre-metastatic niche and other aspects of metastasis. In this review, we provide a general overview of how autophagy modulates cancer metastasis and discuss the significance of new findings for disease management.

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Section: Links Between Autophagy Epithelial-mesenchymal Transition Amentioning

confidence: 99%

Autophagy in cancer metastasis

2016

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“…161 Interestingly, ULK2, which phosphorylates the BECN-1 initiation complex, may also promote EMT in lung cancer cells. 162 Similarly, cisplatin treatment activates autophagy in nasopharyngeal carcinoma, and autophagy inhibition impairs EMT in this progression. 163…”

Section: Autophagy and The Hallmarks Of Cancermentioning

confidence: 99%

Autophagy and Hallmarks of Cancer

et al. 2018

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Autophagy is a catabolic program that is responsible for the degradation of dysfunctional or unnecessary proteins and organelles to maintain cellular homeostasis. Mechanistically, it involves the formation of double-membrane autophagosomes that sequester cytoplasmic material and deliver it to lysosomes for degradation. Eventually, the material is recycled back to the cytoplasm. Abnormalities of autophagy often lead to human diseases, such as neurodegeneration and cancer. In the case of cancer, increasing evidence has revealed the paradoxical roles of autophagy in both tumor inhibition and tumor promotion. Here, we summarize the context-dependent role of autophagy and its complicated molecular mechanisms in the hallmarks of cancer. Moreover, we discuss how therapeutics targeting autophagy can counter malignant transformation and tumor progression. Overall, the findings of studies discussed here shed new light on exploiting the complicated mechanisms of the autophagic machinery and relevant small-molecule modulators as potential antitumor agents to improve therapeutic outcomes.

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“…Certaines études suggèrent que l'autophagie favoriserait l'invasion et la migration des cellules tumorales en permettant la TEM, notamment dans les cholangiocarcinomes (tumeur épithéliale des voies biliaires) et le cancer du poumon [22,23], et qu'elle constituerait, dans ce contexte, un marqueur de mauvais pronostic. Il a également été proposé qu'après la TEM, l'autophagie protège les cellules cancéreuses métastatiques de l'anoïkis, un processus de mort cellulaire induit par le détachement des cellules de leur support matriciel.…”

Section: Rôle Pro-métastatiqueunclassified

L’autophagie : le yin et le yang des cancers

Joffre¹,

Djavaheri-Mergny²,

Pattingre³

et al. 2017

Med Sci (Paris)

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Autophagy is a self-cannibalism process essential for tissue homeostasis, which can be activated following different environmental stressful conditions. In normal cells, autophagy could act as a brake to prevent tumorigenesis, but cancer cells are able to hijack this process to their own benefit, to promote tumor growth and/or tumor resistance to anti-cancer therapies. Scientists and clinicians attempt to modulate this process to improve therapies, using autophagy inhibitors or activators, some of them being tested currently in clinical trials against several types of tumors. Thus, it appears that autophagy is at the center of a showdown between cancer cells and anti-cancer therapies. In this review, we focus on the mechanisms by which autophagy could be either the yin or the yang of cancers.

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Uncoordinated 51‐like kinase 2 signaling pathway regulates epithelial‐mesenchymal transition in A549 lung cancer cells

Cited by 34 publications

References 41 publications

Autophagy in cancer metastasis

Autophagy in cancer metastasis

Autophagy and Hallmarks of Cancer

L’autophagie : le yin et le yang des cancers

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