Energetic adaptations: Metabolic control of endocytic membrane traffic

Rahmani, Sadia; Defferrari, Marina S.; Wakarchuk, Warren W.; Antonescu, Costin N.

doi:10.1111/tra.12705

Cited by 20 publications

(22 citation statements)

References 297 publications

(330 reference statements)

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“…In addition to phosphorylation, ubiquitination events play a critical role in regulating the uptake of specific cargo proteins. Moreover, recent data suggest that both endocytosed cargo proteins and endocytic factors such as AP180 and AAK1 (reviewed in [119]) can also be subject to modification by carbohydrates such as O-GlcNAc that may regulate endocytosis by so far unknown mechanisms. Aside from these post-translational mechanisms, the regulation of endocytosis at the transcriptional level including the possible role of alternative splicing is only now starting to be appreciated.…”

Section: Discussionmentioning

confidence: 99%

Endocytosis in the adaptation to cellular stress

López-Hernández¹,

Haucke²,

Maritzen³

2020

CST

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Cellular life is challenged by a multitude of stress conditions, triggered for example by alterations in osmolarity, oxygen or nutrient supply. Hence, cells have developed sophisticated stress responses to cope with these challenges. Some of these stress programs such as the heat shock response are understood in great detail, while other aspects remain largely elusive including potential stress-dependent adaptations of the plasma membrane proteome. The plasma membrane is not only the first point of encounter for many types of environmental stress, but given the diversity of receptor proteins and their associated molecules also represents the site at which many cellular signal cascades originate. Since these signaling pathways affect virtually all aspects of cellular life, changes in the plasma membrane proteome appear ideally suited to contribute to the cellular adaptation to stress. The most rapid means to alter the cell surface proteome in response to stress is by alterations in endocytosis. Changes in the overall endocytic flux or in the endocytic regulation of select proteins conceivably can help to counteract adverse environmental conditions. In this review we summarize recent data regarding stress-induced changes in endocytosis and discuss how these changes might contribute to the cellular adaptation to stress in different systems. Future studies will be needed to uncover the underlying mechanisms in detail and to arrive at a coherent picture.

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“…AMPK also phosphorylates proteins involved in the control of CME including, clathrin heavy chain, AP2 b2 subunit, dynamin 1, some other traffic coat proteins such as PTRF/cavin or Sec23/24, and several Rab proteins (reviewed in Ref. [92]). Interestingly, AMPK has been described as a target of cell cycle regulators.…”

Section: Cell Cycle Regulators Influence the Intertwine Between Endolysosomal Pathways And Metabolismmentioning

confidence: 99%

The multifaceted role of cell cycle regulators in the coordination of growth and metabolism

et al. 2020

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Adapting to changes in nutrient availability and environmental conditions is a fundamental property of cells. This adaptation requires a multi-directional coordination between metabolism, growth, and the cell cycle regulators (consisting of the family of cyclin-dependent kinases (CDKs), their regulatory subunits known as cyclins, CDK inhibitors, the retinoblastoma family members, and the E2F transcription factors). Deciphering the mechanisms accountable for this coordination is crucial for understanding various patho-physiological processes. While it is well established that metabolism and growth affect cell division, this review will focus on recent observations that demonstrate how cell cycle regulators coordinate metabolism, cell cycle progression, and growth. We will discuss how the cell cycle regulators directly regulate metabolic enzymes and pathways and summarize their involvement in the endolysosomal pathway and in the functions and dynamics of mitochondria.

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“…USMB treatment leads to a reduction in ATP levels within the cell, and AMPK is required for restoring cellular ATP within 2 h following USMB treatment ( Figure 4 ). There are several mechanisms by which AMPK may promote metabolic adaptation resulting in replenishing of ATP levels (Herzig and Shaw, 2018; Rahmani et al, 2019). For instance, AMPK activation increases glucose uptake and promotes glycolysis, by acutely increasing the transport of glucose via facilitative glucose transporters such as GLUT1 (Wu et al, 2013) and phosphorylation of phosphofructokinase 2 (Marsin et al, 2000; Wu and Wei, 2012) as well as by transcriptional regulation of various glycolytic enzymes (Faubert et al, 2013; Marsin et al, 2000; Wu and Wei, 2012).…”

Section: Discussionmentioning

confidence: 99%

AMP-activated protein kinase (AMPK) is required for recovery from metabolic stress induced by ultrasound microbubble treatment

Uchenunu

Botelho

et al. 2022

Preprint

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Ultrasound and microbubbles (USMB) is a promising strategy for cancer therapy. USMB can induce a variety of effects on cells including transient formation of plasma membrane pores (sonoporation) and enhanced endocytosis, which enhance drug delivery, and can also lead to enhanced cell death. However, the outcomes of USMB on cell physiology are heterogeneous, in that USMB elicits cell death in a proportion of cells while exerting minimal effects on others. This suggests that mechanisms of adaptation following USMB allow some cells to survive and/or proliferate. The molecular mechanisms of adaptation to USMB-induced stress remain poorly understood, thus potentially hindering broad therapeutic applications of USMB. Herein, we used several triple negative breast cancer cells to study the effect of USMB-induced metabolite stress and the role of AMPK as a response to this stress. We found that USMB alters steady-state levels of amino acids, glycolytic intermediates, and citric acid cycle intermediates. USMB treatment acutely reduces ATP levels and stimulates AMP-activated protein kinase (AMPK) phosphorylation and activation. Further, AMPK is required to restore ATP levels in cells that survived the initial insult and support cell proliferation post-USMB treatment. These results suggest that AMPK and metabolic perturbations are likely determinants of the anti-neoplastic efficacy of USMB treatment.

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“…AMPK regulates diverse metabolic cellular processes, and also endocytic traffic during metabolic stress. When it is activated, it inhibits energy demanding processes and enhances catabolic reaction to generate ATP (Rahmani et al, 2019). AMPK can both suppress but also promote tumor growth (Hardie, 2015).…”

Section: Macropinocytosis and Cancer Cell Proliferationmentioning

confidence: 99%

Intracellular Transport in Cancer Metabolic Reprogramming

Sneeggen

Guadagno

Progida

2020

Front. Cell Dev. Biol.

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Tumor progression is a complex process consisting of several steps characterized by alterations in cellular behavior and morphology. These steps include uncontrolled cell division and proliferation, invasiveness and metastatic ability. Throughout these phases, cancer cells encounter a changing environment and a variety of metabolic stress. To meet their needs for energy while they proliferate and survive in their new environment, tumor cells need to continuously fine-tune their metabolism. The connection between intracellular transport and metabolic reprogramming during cancer progression is emerging as a central process of cellular adaptation to these changes. The trafficking of proteolytic enzymes, surface receptors, but also the regulation of downstream pathways, are all central to cancer progression. In this review, we summarize different hallmarks of cancer with a special focus on the role of intracellular trafficking in cell proliferation, epithelial to mesenchymal transition as well as invasion. We will further emphasize how intracellular trafficking contributes to the regulation of energy consumption and metabolism during these steps of cancer progression.

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“…In the third review by Rahmani et al, we examine the reciprocal relationship of how signals derived from cell metabolism impact endocytic membrane traffic, with emphasis on cell autonomous metabolic cues. Focusing largely on mammalian cells, this review delineates how sufficiency or limitations of specific nutrients, including glucose, ATP and amino acids, are sensed, such as by triggering changes in activity of signaling kinases such as AMP‐activated protein kinase (AMPK) or mechanistic target of rapamycin (mTOR), which in turn regulate endocytic membrane traffic in a variety of tissues and cell types.…”

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confidence: 99%