Non-canonical processes that shape the cell migration landscape

Majumdar, Ritankar; Steen, Kaylee; Parent, Carole A.

doi:10.1016/j.ceb.2018.12.013

Cited by 12 publications

(14 citation statements)

References 98 publications

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“…Interestingly, KRT19 KO cells showed more motility than parental cells on a rigid substrate despite fewer focal adhesions and actin stress fibers. Although focal adhesions and associated stress fibers play important roles in mechanotransduction and cell migration, cell migration is a complex process with multiple types of cell migrations not involving focal adhesions (43,44). In fact, stable focal adhesions and stress fibers can inhibit cell motility due to the burden of reorganizing such structures (42).…”

Section: Discussionmentioning

confidence: 99%

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Morphology, Motility, and Cytoskeletal Architecture of Breast Cancer Cells Depend on Keratin 19 and Substrate

et al. 2020

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Cancer cells gain motility through events that accompany modulation of cell shape and include altered expression of keratins. However, the role of keratins in change of cancer cell architecture is not well understood. Therefore, we ablated the expression of keratin 19 (K19) in breast cancer cells of the MDA-MB-231 cell line and found that cells lacking K19 become more elongated in culture, with morphological reversion toward the parental phenotype upon transduction of KRT19. Also, the number of actin stress fibers and focal adhesions were significantly reduced in KRT19 knockout (KO) cells. The altered morphology of KRT19 KO cells was then characterized quantitatively using digital holographic microscopy (DHM), which not only confirmed the phenotypic change of KRT19 KO cells but also identified that the K19-dependent morphological change is dependent on the substrate type. A new quantitative method of single cell analysis from DHM, via average phase difference maps, facilitated evaluation of K19-substrate interactive effects on cell morphology. When plated on collagen substrate, KRT19 KO cells were less elongated and resembled parental cells. Assessing single cell motility further showed that while KRT19 KO cells moved faster than parental cells on a rigid surface, this increase in motility became abrogated when cells were plated on collagen. Overall, our study suggests that K19 inhibits cell motility by regulating cell shape in a substrate-dependent manner. Thus, this study provides a potential basis for the altered expression of keratins associated with change in cell shape and motility of cancer cells.

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Section: Discussionmentioning

confidence: 99%

“…Altered cell morphology is linked to different degrees and modes of cell motility (43,44). Therefore, we decided to assess the impact of substrate variation on cell motility of KRT19 KO cells.…”

Section: Substrate-dependent Inhibition Of Cell Motility By K19mentioning

confidence: 99%

Morphology, Motility, and Cytoskeletal Architecture of Breast Cancer Cells Depend on Keratin 19 and Substrate

et al. 2020

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“…As far as the dendritic-cell experiment is concerned, immune cells release molecules towards the extracellular milieu, which could steer the migration of adjacent cells [15]. Indeed, the release of vesicles or small molecules to extracellular milieu as a mechanism of paracrine cell communication allows coordinated migration in a contactindependent manner in other cellular systems [14,11].…”

Section: Discussionmentioning

confidence: 99%

A statistical inference approach to reconstruct intercellular interactions in cell migration experiments

et al. 2020

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Migration of cells can be characterized by two, prototypical types of motion: individual and collective migration. We propose a statistical-inference approach designed to detect the presence of cell-cell interactions that give rise to collective behaviors in cell-motility experiments. Such inference method has been first successfully tested on synthetic motional data, and then applied to two experiments. In the first experiment, cell migrate in a wound-healing model: when applied to this experiment, the inference method predicts the existence of cellcell interactions, correctly mirroring the strong intercellular contacts which are present in the experiment. In the second experiment, dendritic cells migrate in a chemokine gradient. Our inference analysis does not provide evidence for interactions, indicating that cells migrate by sensing independently the chemokine source. According to this prediction, we speculate that mature dendritic cells disregard inter-cellular signals that could otherwise delay their arrival to lymph vessels.

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“…As a consequence, mitochondrial repositioning in the cortical cytoskeleton sustains the turnover of focal adhesion complexes and therefore facilitates cell migration and invasion [158][159][160]. Mechanistically, Caino et al established that cancer cells reprogram a network of proteins involved in mitochondrial intracellular trafficking centered on syntaphilin to shuttle mitochondria to the cortical cytoskeleton and sustain metastasis [161,162].…”

Section: Mitochondrial Dynamicsmentioning

confidence: 99%

Apoptosis – Fueling the oncogenic fire

2020

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Apoptosis, the most extensively studied form of programmed cell death, is essential for organismal homeostasis. Apoptotic cell death has widely been reported as a tumor suppressor mechanism. However, recent studies have shown that apoptosis exerts noncanonical functions and may paradoxically promote tumor growth and metastasis. The hijacking of apoptosis by cancer cells may arise at different levels, either via the interaction of apoptotic cells with their local or distant microenvironment, or through the abnormal pro‐oncogenic roles of the main apoptosis effectors, namely caspases and mitochondria, particularly upon failed apoptosis. In this review, we highlight some of the recently described mechanisms by which apoptosis and these effectors may promote cancer aggressiveness. We believe that a better understanding of the noncanonical roles of apoptosis may be crucial for developing more efficient cancer therapies.

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Non-canonical processes that shape the cell migration landscape

Cited by 12 publications

References 98 publications

Morphology, Motility, and Cytoskeletal Architecture of Breast Cancer Cells Depend on Keratin 19 and Substrate

Morphology, Motility, and Cytoskeletal Architecture of Breast Cancer Cells Depend on Keratin 19 and Substrate

A statistical inference approach to reconstruct intercellular interactions in cell migration experiments

Apoptosis – Fueling the oncogenic fire

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