Macropinocytosis and Cancer: From Tumor Stress to Signaling Pathways

Lambies, Guillem; Commisso, Cosimo

doi:10.1007/978-3-030-94004-1_2

Cited by 21 publications

(13 citation statements)

References 114 publications

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“…In vitro studies reveal that cancer cells utilize albumin as an alternative source of nutrients (Recouvreux and Commisso, 2017 ). An in vivo study shows that PDAC cells can take in albumin and use the amino acids it contains in other metabolic pathways, which normal cells can’t do (Lambies and Commisso, 2022 ).…”

Section: Metabolic Pathways Associated With Cancer Progressionmentioning

confidence: 99%

Recent progress in the development of nanomaterials targeting multiple cancer metabolic pathways: a review of mechanistic approaches for cancer treatment

Zhang

Zhai²,

et al. 2023

Drug Delivery

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Cancer is a very heterogeneous disease, and uncontrolled cell division is the main characteristic of cancer. Cancerous cells need a high nutrition intake to enable aberrant growth and survival. To do so, cancer cells modify metabolic pathways to produce energy and anabolic precursors and preserve redox balance. Due to the importance of metabolic pathways in tumor growth and malignant transformation, metabolic pathways have also been given promising perspectives for cancer treatment, providing more effective treatment strategies, and target-specific with minimum side effects. Metabolism-based therapeutic nanomaterials for targeted cancer treatment are a promising option. Numerous types of nanoparticles (NPs) are employed in the research and analysis of various cancer therapies. The current review focuses on cutting-edge strategies and current cancer therapy methods based on nanomaterials that target various cancer metabolisms. Additionally, it highlighted the primacy of NPs-based cancer therapies over traditional ones, the challenges, and the future potential.

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Section: Metabolic Pathways Associated With Cancer Progressionmentioning

confidence: 99%

Recent progress in the development of nanomaterials targeting multiple cancer metabolic pathways: a review of mechanistic approaches for cancer treatment

Zhang

Zhai²,

et al. 2023

Drug Delivery

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“…Whereas phagocytosis activation depends on phagocytic targets/cargo ligating cognate phagocytic receptors, the activation of macropinocytosis does not. Macropinocytosis may be triggered by growth factors (e.g., epidermal growth factor) and Ca +2 or occur autonomously (Canton, 2022 ; Lambies and Commisso, 2022 ; Palm, 2022 ). Nonetheless, macropinocytosis and phagocytosis share many signaling molecules that are involved in directing the cytoskeleton to produce the mechanical forces that drive the structural changes on which they depend; e.g., K-Ras, PI3K, Rac, PLC, PIP 3 and PIP 2 , and PKC; (Swanson, 2008 ; Zhang and Commisso, 2019 ; Lambies and Commisso, 2022 ; Palm, 2022 ).…”

Section: Gal-3 Controls Macropinocytosis In Some Types Of Cancer Cellsmentioning

confidence: 99%

Galectin-3 (MAC-2) controls phagocytosis and macropinocytosis through intracellular and extracellular mechanisms

Rotshenker

2022

Front. Cell. Neurosci.

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Galectin-3 (Gal-3; formally named MAC-2) is a β-galactoside-binding lectin. Various cell types produce Gal-3 under either normal conditions and/or pathological conditions. Gal-3 can be present in cells' nuclei and cytoplasm, secreted from producing cells, and associated with cells' plasma membranes. This review focuses on how Gal-3 controls phagocytosis and macropinocytosis. Intracellular and extracellular Gal-3 promotes the phagocytosis of phagocytic targets/cargo (e.g., tissue debris and apoptotic cells) in “professional phagocytes” (e.g., microglia and macrophages) and “non-professional phagocytes” (e.g., Schwann cells and astrocytes). Intracellularly, Gal-3 promotes phagocytosis by controlling the “eat me” signaling pathways that phagocytic receptors generate, directing the cytoskeleton to produce the mechanical forces that drive the structural changes on which phagocytosis depends, protrusion and then retraction of filopodia and lamellipodia as they, respectively, engulf and then internalize phagocytic targets. Extracellularly, Gal-3 promotes phagocytosis by functioning as an opsonin, linking phagocytic targets to phagocytic receptors, activating them to generate the “eat me” signaling pathways. Macropinocytosis is a non-selective endocytic mechanism that various cells use to internalize the bulk of extracellular fluid and included materials/cargo (e.g., dissolved nutrients, proteins, and pathogens). Extracellular and intracellular Gal-3 control macropinocytosis in some types of cancer. Phagocytosed and macropinocytosed targets/cargo that reach lysosomes for degradation may rupture lysosomal membranes. Damaged lysosomal membranes undergo either repair or removal by selective autophagy (i.e., lysophagy) that intracellular Gal-3 controls.

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“…The requirement of macropinocytosis for Wnt signaling is revealed, for example, by the decrease in nuclear β-catenin when colorectal cancer (CRC) cells mutant for APC were treated with macropinocytosis inhibitors such as the derivative of the diuretic Amiloride known as 5-(N-Ethyl-N-isopropyl) Amiloride (EIPA) (Tejeda-Muñoz et al, 2019;De Robertis, 2022a, 2022b;). Macropinocytosis is emerging in the field as a promising target for cancer treatment (Lambies and Commisso, 2022). In addition, it has been found that the macropinocytosis induced by Wnt signaling causes significant lysosome acidification and activation (Albrecht et al, 2020).…”

Section: Introductionmentioning

confidence: 99%

The PMA Phorbol Ester Tumor Promoter Increases Canonical Wnt Signaling Via Macropinocytosis

Tejeda-Muñoz,

Azbazdar,

Monka

et al. 2023

Preprint

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Activation of the Wnt pathway lies at the core of many human cancers. Interestingly, Wnt, cell adhesion, and macropinocytosis are often active in the same processes, and understanding how Wnt signaling and membrane trafficking cooperate should improve our understanding of embryonic development and cancer. Here we show that a macropinocytosis activator, the tumor promoter Phorbol 12-myristate 13-acetate (PMA), enhances Wnt signaling. Experiments using the Xenopus embryo as an in vivo model showed marked cooperation between the PMA phorbol ester and Wnt signaling, which was blocked by inhibitors of macropinocytosis, Rac1 activity, and lysosome acidification. The crosstalk between canonical Wnt, the Protein Kinase C (PKC) pathway, focal adhesions, lysosomes, and macropinocytosis suggests possible therapeutic targets for cancer progression in Wnt-driven cancers.

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Macropinocytosis and Cancer: From Tumor Stress to Signaling Pathways

Cited by 21 publications

References 114 publications

Recent progress in the development of nanomaterials targeting multiple cancer metabolic pathways: a review of mechanistic approaches for cancer treatment

Recent progress in the development of nanomaterials targeting multiple cancer metabolic pathways: a review of mechanistic approaches for cancer treatment

Galectin-3 (MAC-2) controls phagocytosis and macropinocytosis through intracellular and extracellular mechanisms

The PMA Phorbol Ester Tumor Promoter Increases Canonical Wnt Signaling Via Macropinocytosis

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