LC3C-Mediated Autophagy Selectively Regulates the Met RTK and HGF-Stimulated Migration and Invasion

Bell, Emily; Coelho, Paula P.; Ratcliffe, Colin D.H.; Rajadurai, Charles V.; Peschard, Pascal; Vaillancourt, Richard; Zuo, Dongmei; Park, Morag

doi:10.1016/j.celrep.2019.11.063

Cited by 39 publications

(37 citation statements)

References 106 publications

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“…Interestingly, optimal Met signalling requires non-canonical ATG8 lipidation on single membranes in various cancer lines [ 106 ]. On the other hand, autophagy may also suppress Met signalling by targeting its degradation through binding with LC3C in breast and cervical cancer cell lines [ 110 ]. HIF2 α stabilization can reduce LC3C expression [ 111 ]; therefore, it could be hypothesized that enhanced expression of HIF in hypoxic tumours, such as glioblastoma, could release Met from LC3C-mediated downregulation [ 110 ].…”

Section: Autophagy and Glioblastoma Invasionmentioning

confidence: 99%

“…On the other hand, autophagy may also suppress Met signalling by targeting its degradation through binding with LC3C in breast and cervical cancer cell lines [ 110 ]. HIF2 α stabilization can reduce LC3C expression [ 111 ]; therefore, it could be hypothesized that enhanced expression of HIF in hypoxic tumours, such as glioblastoma, could release Met from LC3C-mediated downregulation [ 110 ]. Given that autophagy can both stimulate and inhibit Met signalling in various cancer cell lines, it would be interesting to determine how this regulatory network can implicate invasion of Met-expressing glioblastoma cells.…”

Section: Autophagy and Glioblastoma Invasionmentioning

confidence: 99%

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The impact of autophagy during the development and survival of glioblastoma

Simpson

Gammoh

2020

Open Biol.

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Glioblastoma is the most common and aggressive adult brain tumour, with poor median survival and limited treatment options. Following surgical resection and chemotherapy, recurrence of the disease is inevitable. Genomic studies have identified key drivers of glioblastoma development, including amplifications of receptor tyrosine kinases, which drive tumour growth. To improve treatment, it is crucial to understand survival response processes in glioblastoma that fuel cell proliferation and promote resistance to treatment. One such process is autophagy, a catabolic pathway that delivers cellular components sequestered into vesicles for lysosomal degradation. Autophagy plays an important role in maintaining cellular homeostasis and is upregulated during stress conditions, such as limited nutrient and oxygen availability, and in response to anti-cancer therapy. Autophagy can also regulate pro-growth signalling and metabolic rewiring of cancer cells in order to support tumour growth. In this review, we will discuss our current understanding of how autophagy is implicated in glioblastoma development and survival. When appropriate, we will refer to findings derived from the role of autophagy in other cancer models and predict the outcome of manipulating autophagy during glioblastoma treatment.

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Section: Autophagy and Glioblastoma Invasionmentioning

confidence: 99%

Section: Autophagy and Glioblastoma Invasionmentioning

confidence: 99%

The impact of autophagy during the development and survival of glioblastoma

Simpson

Gammoh

2020

Open Biol.

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“…Autophagy is a highly conserved self-digestion process that plays a crucial role in maintaining cellular homeostasis in response to nutrient depletion or other stresses, such as accumulation of damaged organelles, unneeded protein aggregation, and invading microbes (14). Autophagy may have varying effects on different pathogens and hosts.…”

Section: Introductionmentioning

confidence: 99%

Taurine Alleviates Streptococcus uberis-Induced Inflammation by Activating Autophagy in Mammary Epithelial Cells

Wang

Lan

et al. 2021

Front. Immunol.

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Streptococcus uberis infection can cause serious inflammation and damage to mammary epithelial cells and tissues that can be significantly alleviated by taurine. Autophagy plays an important role in regulating immunity and clearing invasive pathogens and may be regulated by taurine. However, the relationships between taurine, autophagy, and S. uberis infection remain unclear. Herein, we demonstrate that taurine augments PTEN activity and inhibits Akt/mTOR signaling, which decreases phosphorylation of ULK1 and ATG13 by mTOR and activates autophagy. Activating autophagy accelerates the degradation of intracellular S. uberis, reduces intracellular bacterial load, inhibits over-activation of the NF-κB pathway, and alleviates the inflammation and damage caused by S. uberis infection. This study increases our understanding of the mechanism through which taurine regulates autophagy and is the first to demonstrate the role of autophagy in S. uberis infected MAC-T cells. Our study also provides a theoretical basis for employing nutritional elements (taurine) to regulate innate immunity and control S. uberis infection. It also provides theoretical support for the development of prophylactic strategies for this important pathogen.

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“…In this regard, a major driver of OXPHOS is PGC-1alpha, which is not oncogenically altered in cancer, but its expression level controls mitochondrial biogenesis [40]. Likewise, the MET receptor tyrosine kinase, a major driver of cell motility and invasion, is regulated post-translationally at multiple levels, including degradation by selective autophagy, which is itself affected by oxygen availability and the tumor suppressor VHL [59].…”

Section: Plasticity and Hybrid Programsmentioning

confidence: 99%