Decoding leader cells in collective cancer invasion

Mercedes, Samuel A Vilchez; Bocci, Federico; Levine, Herbert; Onuchic, José N.; Jolly, Mohit Kumar; Wong, Pak Kin

doi:10.1038/s41568-021-00376-8

Cited by 109 publications

(93 citation statements)

References 160 publications

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“…Rac1 activates formation of lamellipodia and membrane ruffles, while RhoA controls actomyosin contraction and cell contractility. 33 , 34 Rac1 and RhoA work coordinately to regulate actin reorganization which is essential for cell migration through activation of WAVE1, a downstream effector for Rac. 35 , 36 As expected, WAVE1 was expressed in pig endometrium on gestational day 15, suggesting that WAVE1 was activated by active Rac1.…”

Section: Discussionmentioning

confidence: 99%

“…As a cell‐cell adhesion molecule of epithelial cells, E‐cadherin mediates adhesion junction which plays a vital role in collective cell migration. 33 , 41 Previous studies have revealed that the adhesion junction stability is dynamically tuned, allowing the considerable rearrangements of cells during collective cell migration, but the corresponding mechanisms remain to be elucidated. 42 , 43 The role of N‐glycosylation in E‐cadherin‐mediated epithelial cell‐to‐cell adhesion, E‐cadherin cellular trafficking and E‐cadherin‐dependent signalling has been confirmed in previous studies.…”

Section: Discussionmentioning

confidence: 99%

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Glycomics reveal that ST6GAL1‐mediated sialylation regulates uterine lumen closure during implantation

et al. 2021

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Objectives Implantation failure is a major cause of prenatal mortality. The uterine lumen closure contributes to embryo adhesion to the uterus, but its underlying mechanisms are largely unknown. Our previous study has reported that endometrial fold extension can lead to uterine lumen closure in pigs. The objective of this study was to reveal molecular mechanisms of the uterine lumen closure by characterizing the molecular basis of the endometrial fold extension during implantation in pigs. Materials and methods Uterine and endometrium tissues during implantation were collected in pigs. MALDI‐TOF MS was used to characterize the N‐glycomic profiles. Histochemistry, siRNA transfection, Western blotting, lectin immumoprecipitation, mass spectrometry and assays of wounding healing and cell aggregation were performed to investigate the molecular basis. Results We observed that uterine luminal epithelium (LE) migrated collectively during endometrial fold extension. For the first time, we identified a large number of N‐glycan compositions from endometrium during implantation using MALDI‐TOF MS. Notably, the α2,6‐linked sialic acid and ST6GAL1 were highly expressed in uterine LE when the endometrial folds extended greatly. Subsequently, the role of ST6GAL1‐mediated 2,6‐sialylation in collective epithelial migration was demonstrated. Finally, we found that ST6GAL1‐mediated α2,6‐sialylation of E‐cadherin may participate in collective migration of uterine LE. Conclusions The study reveals a mechanism of uterine lumen closure by identifying that ST6GAL1‐mediated α2,6‐sialylation of cell adhesion molecules contributes to endometrial fold extension through regulating collective migration of uterine LE.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Glycomics reveal that ST6GAL1‐mediated sialylation regulates uterine lumen closure during implantation

et al. 2021

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“…Cancer cell migration is the key step that allows invasion and colonization of new tissues. The stimulation of this response occurs during the epithelial to mesenchymal transition (EMT) ( 119 , 120 ). Interestingly, dichotomic contribution of PANX1 on cancer cell migration has been reported (summarized in Table 2 ).…”

Section: Role Of Panxs On Migration Of Non-immune Cellsmentioning

confidence: 99%

Pannexin Channel Regulation of Cell Migration: Focus on Immune Cells

et al. 2021

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The role of Pannexin (PANX) channels during collective and single cell migration is increasingly recognized. Amongst many functions that are relevant to cell migration, here we focus on the role of PANX-mediated adenine nucleotide release and associated autocrine and paracrine signaling. We also summarize the contribution of PANXs with the cytoskeleton, which is also key regulator of cell migration. PANXs, as mechanosensitive ATP releasing channels, provide a unique link between cell migration and purinergic communication. The functional association with several purinergic receptors, together with a plethora of signals that modulate their opening, allows PANX channels to integrate physical and chemical cues during inflammation. Ubiquitously expressed in almost all immune cells, PANX1 opening has been reported in different immunological contexts. Immune activation is the epitome coordination between cell communication and migration, as leukocytes (i.e., T cells, dendritic cells) exchange information while migrating towards the injury site. In the current review, we summarized the contribution of PANX channels during immune cell migration and recruitment; although we also compile the available evidence for non-immune cells (including fibroblasts, keratinocytes, astrocytes, and cancer cells). Finally, we discuss the current evidence of PANX1 and PANX3 channels as a both positive and/or negative regulator in different inflammatory conditions, proposing a general mechanism of these channels contribution during cell migration.

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“…1 Furthermore, single cell methods are required for studying cell heterogeneity and multicellular organization of complex biological processes, such as tissue morphogenesis and tumor invasion. 2–4 Imaging techniques, such as fluorescence in situ hybridization (FISH), open a door into studying RNA expression in fixed cells down to the single transcript level. 5,6 Nonetheless, FISH is laborious, applicable only to fixed cells, and difficult to implement in 3D cultures.…”

Section: Introductionmentioning

confidence: 99%