AMPK-induced autophagy as a key regulator of cell migration

Bressan, Cedric; Saghatelyan, Armen

doi:10.1080/15548627.2020.1848120

Cited by 13 publications

(9 citation statements)

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“…Autophagy has recently been found to play an essential role in the regulation of many types of cell migration [35][36][37], but the related mechanisms are not fully understood. Bressan and Saghatelyan showed that AMPKinduced autophagy is a key regulator of cell migration and plays an important role in the recycling of the focal adhesion molecule paxillin [38]. Kenifc and Debnath established that the autophagy cargo receptor NBR1 is an important mediator that supports cell migration; NBR1 interacts with focal adhesions through the ubiquitin binding domain and then targets autophagosomes to FAs, which leads to its disintegration by isolation of FA proteins [39].…”

Section: Discussionmentioning

confidence: 99%

Autophagy Modulates the Migration of Retinal Pericytes Induced by Advanced Glycation End Products

Lin

Zhou

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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Retinal pericyte migration occurs in the early stage of diabetic retinopathy (DR), which is one of the important causes of pericyte loss. Autophagy has been found to play essential roles in the regulation of many types of cell migration. In this study, we explored the relationship between autophagy and retinal pericyte migration. In diabetic rats, the retinas became thinner, and the level of autophagy in each cell layer increased. In the primary culture of bovine retinal pericytes, we found that advanced glycation end products (AGEs) increased the migratory cell ability without influencing cell viability, which also increased the phosphorylation of focal adhesion kinase (FAK) and the expression of matrix metalloproteinase (MMP)-2 and decreased the expression of vinculin. AGEs-induced retinal pericyte autophagy and the inhibition of autophagy with chloroquine significantly inhibited cell migration, reversed AGEs-induced FAK phosphorylation, and changed vinculin and MMP-2 protein expression. These results provide a new insight into the migration mechanism of retinal pericytes. The early control of autophagy has a potential effect on regulating pericyte migration, which may contribute to keeping the integrity of retinal vessels in DR.

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Section: Discussionmentioning

confidence: 99%

Autophagy Modulates the Migration of Retinal Pericytes Induced by Advanced Glycation End Products

Lin

Zhou

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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“…Moreover, AMPK-induced autophagy is a crucial regulator of cell migration [42]. AMPK has been widely recognized as a promising pharmacological target, especially in treating diabetes, obesity, inflammation, and cancer [42,43]. In short, AMPK's role in cells is complex.…”

Section: Discussionmentioning

confidence: 99%

Albumin Paclitaxel Compared with 5-Penfluorouracil, Lobaplatin, and Albumin Paclitaxel Combined with 5-Penfluorouracil in the Treatment of Human Gastric Cancer Cell AGS Line Autophagy and Apoptosis

Cheng

Yang

Wang

et al. 2022

Canadian Journal of Gastroenterology and Hepatology

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Background. Gastric cancer is one of the most common malignant tumors in the world. Albumin paclitaxel (Nab-PTX) is a novel microtubule inhibitor with albumin as the carrier. Several clinical trials are underway in gastric cancer, but the autophagy mechanism of Nab-PTX on gastric cancer is still unclear. The autophagy and apoptosis effects of Nab-PTX compared with 5-pentafluorouracil (5-Fu) and lobaplatin (LBP) in gastric cancer are also unclear. Objective. This article will compare the effects of Nab-PTX, 5-Fu, LBP, and albumin paclitaxel + 5-pentafluorouracil (Nab-PTX + 5-Fu) on AGS cells from the perspective of autophagy and apoptosis, which is to provide new ideas and experimental evidence for gastric cancer. Method. (1) Experimental groups were control (Ctrl), Nab-PTX, 5-Fu, LBP, and Nab-PTX + 5-Fu. (2) CCK-8 assay was used to reflect cell viability and proliferation. (3) The flow cytometry was used to perform the 24-hour apoptosis and cell cycle of each group. (4) Western blot assay was used to investigate autophagy signal proteins LC3I/LC3II, LC3II/LC3I, SQSTM1/p62, Beclin-1, Atg12, Atg5, p-mULK1, p-AMPK, p-mTOR, and apoptosis signal proteins Bax and Bcl-2. Results. Nab-PTX, 5-Fu, LBP, and Nab-PTX + 5-Fu inhibited AGS cells' proliferation and arrested the cell cycle. At the same time, each group increased the apoptosis of AGS cells to various degrees (Nab-PTX + 5-Fu > Nab-PTX > 5-Fu > LBP, respectively). The experimental results showed that Nab-PTX and Nab-PTX + 5-Fu promoted autophagy and apoptosis of AGS cells. The comparison of Nab-PTX, 5-Fu, and LBP between groups revealed that 5-Fu inhibited autophagy and the expression of apoptosis protein Bax. In LBP, abnormal activation of autophagy downstream, blocking of autophagy flow, abnormal increase of ATG12, and increased expression of apoptosis protein Bax occurred. Further study found that the autophagy upstream mechanism is different. Conclusion. Nab-PTX, 5-Fu, LBP, and Nab-PTX + 5-Fu can inhibit cell proliferation, promote cell apoptosis, and induce the difference in autophagy expression. The autophagy difference of this antitumor drug may be related to its inducing apoptosis. Meanwhile, Nab-PTX has a better antitumor effect than 5-Fu and LBP in gastric cancer, and the combination of Nab-PTX + 5-Fu has more antitumor advantages.

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“…The Vps15 part of the class III PI3K complex is also involved in the stabilization of cytoskeleton dynamics by decreasing the activity of Pak1, an effector of Rac1 and Cdc42 (Gstrein et al, 2018). We recently showed that the dynamic interplay between ATP/ADP levels and autophagy is required to sustain neuronal migration in the postnatal and adult brain (Bressan and Saghatelyan, 2020;. A decrease in ATP levels during the migratory phase causes cells to enter into the stationary period and activates AMPK.…”

Section: Autophagymentioning

confidence: 99%

Intrinsic Mechanisms Regulating Neuronal Migration in the Postnatal Brain

Bressan

Saghatelyan

2021

Front. Cell. Neurosci.

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Neuronal migration is a fundamental brain development process that allows cells to move from their birthplaces to their sites of integration. Although neuronal migration largely ceases during embryonic and early postnatal development, neuroblasts continue to be produced and to migrate to a few regions of the adult brain such as the dentate gyrus and the subventricular zone (SVZ). In the SVZ, a large number of neuroblasts migrate into the olfactory bulb (OB) along the rostral migratory stream (RMS). Neuroblasts migrate in chains in a tightly organized micro-environment composed of astrocytes that ensheath the chains of neuroblasts and regulate their migration; the blood vessels that are used by neuroblasts as a physical scaffold and a source of molecular factors; and axons that modulate neuronal migration. In addition to diverse sets of extrinsic micro-environmental cues, long-distance neuronal migration involves a number of intrinsic mechanisms, including membrane and cytoskeleton remodeling, Ca2+ signaling, mitochondria dynamics, energy consumption, and autophagy. All these mechanisms are required to cope with the different micro-environment signals and maintain cellular homeostasis in order to sustain the proper dynamics of migrating neuroblasts and their faithful arrival in the target regions. Neuroblasts in the postnatal brain not only migrate into the OB but may also deviate from their normal path to migrate to a site of injury induced by a stroke or by certain neurodegenerative disorders. In this review, we will focus on the intrinsic mechanisms that regulate long-distance neuroblast migration in the adult brain and on how these pathways may be modulated to control the recruitment of neuroblasts to damaged/diseased brain areas.

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AMPK-induced autophagy as a key regulator of cell migration

Cited by 13 publications

References 1 publication

Autophagy Modulates the Migration of Retinal Pericytes Induced by Advanced Glycation End Products

Autophagy Modulates the Migration of Retinal Pericytes Induced by Advanced Glycation End Products

Albumin Paclitaxel Compared with 5-Penfluorouracil, Lobaplatin, and Albumin Paclitaxel Combined with 5-Penfluorouracil in the Treatment of Human Gastric Cancer Cell AGS Line Autophagy and Apoptosis

Intrinsic Mechanisms Regulating Neuronal Migration in the Postnatal Brain

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