Rebooting the collagen gel: Artificial hydrogels for the study of epithelial mesenchymal transformation

Dettman, Robert W.; Simon, Hans Georg

doi:10.1002/dvdy.24560

Cited by 5 publications

(4 citation statements)

References 57 publications

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“…The interstitial Col-I fibril lattices function as both a cell scaffold and a barrier to prevent cell migration in cancer invasion process (6,66). Furthermore, EMT induction via adhesion to Col-I is thought to enhance cancer invasion (32).…”

Section: Discussionmentioning

confidence: 99%

“…In vivo, many kinds of cells are found resting proliferation within Col-I fibrils containing matrix, while, cellextracellular matrix (ECM) interactions are essential for cell movement (1). For a long while, Col-I has been widely studied and used as a cell culture substrate (1)(2)(3)(4)(5)(6)(7). Typically, Col-I is solubilized under acidic conditions and extracted from animal tissues.…”

Section: Introductionmentioning

confidence: 99%

“…Sometimes, the former is called "2D culture substrate" and the latter is "3D culture substrate" respectively. Recently fibril-forming Col-I has been used as novel hydrogels (5) and the history of the collagen gel culture assay has been reviewed (6).…”

Section: Introductionmentioning

confidence: 99%

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Adhesion to type I collagen fibrous gels induces E- to N-cadherin switching without other EMT-related phenotypes in lung carcinoma cell A549

Fujisaki

Futaki²,

Yamada

et al. 2020

Preprint

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In culture system, environmental factors, such as increasing exogenous growth factors and adhesion to type I collagen (Col-I) induce epithelial-to-mesenchymal transition (EMT) in cells. Col-I molecules maintain a non-fibril form under acidic conditions, and they reassemble into fibrils under physiological conditions. Col-I fibrils often assemble to form three-dimensional gels. The gels and non-gel-form of Col-I can be utilized as culture substrates and different gel-forming state often elicit different cell behaviors. However, gel-form dependent effects on cell behaviors, including EMT induction, remain unclear. EMT induction in lung cancer cell line A549 has been reported via adhesion to Col-I but the effects of gel form dependency are unelucidated. This study investigated the changes in EMT-related behaviors in A549 cells cultured on Col-I gels.We examined cell morphology, proliferation, single-cell migration and expression of EMT-related features in A549 cells cultured on gels or non-gel form of Col-I and non-treated dish with or without transforming growth factor (TGF)-β1. On Col-I gels, some cells kept cell–cell contacts and formed clusters, others maintained single-cell form. In cell–cell contact regions, E-cadherin expression was downregulated, whereas that of N-cadherin was upregulated. Vimentin and integrins α2 and β1 expression were not increased. In TGF-β1-treated A549 cells, cadherin switched from E- to N-cadherin. Their morphology changed to a mesenchymal form and cells scattered with no cluster formation. Vimentin, integrins α2 and β1 expression were upregulated. Thus, we concluded that culture on Col-I fibrous gels induced E- to N-cadherin switching without other EMT-related phenotypes in A549 cells.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Adhesion to type I collagen fibrous gels induces E- to N-cadherin switching without other EMT-related phenotypes in lung carcinoma cell A549

Fujisaki

Futaki²,

Yamada

et al. 2020

Preprint

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show abstract

“…EMT refers to the phenomenon of epithelial cells transforming into mesenchymal cells under specific physiological and pathological conditions ( 21 , 22 ). Cells may lose their connection and polarity, change in morphology, and their migration ability may be enhanced, thus gaining invasion and metastasis abilities ( 23 , 24 ). It has been reported that although melanocytes are not traditional epithelial components, there is EMT in the process of melanoma invading dermal stroma ( 25 ).…”

Section: Introductionmentioning

confidence: 99%

Mechanisms of JAK‑STAT signaling pathway mediated by CXCL8 gene silencing on epithelial‑mesenchymal transition of human cutaneous melanoma cells

Yuan²,

2020

Oncol Lett

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Effect of CXCL8 gene silencing-mediated JAK-STAT signaling pathway on epithelial-mesenchymal transition (EMT) of human cutaneous melanoma cells was explored. Eighty patients with cutaneous melanoma were enrolled in the study. Cells were transfected accordingly and divided into five groups: The blank group (human cutaneous melanoma cells), NC group (human cutaneous melanoma cells + blank vector plasmid transfection), CXCL8 siRNA group (human cutaneous melanoma cells + CXCL8 silent expression vector plasmid transfection), AG490 group (human cutaneous melanoma cells + JAK-STAT signal pathway inhibitor transfection), CXCL8 siRNA + AG490 group (human cutaneous melanoma cells + JAK-STAT signaling pathway inhibitor + CXCL8 silent expression vector plasmid transfection). The expression levels of CXCL8, JAK2, STAT3, epithelial cadherin (E-cadherin), neurotrophic cadherin (N-cadherin) and vimentin in tissues and cells were detected by RT-qPCR and western blot analysis. CCK-8 and flow cytometry were used to detect cell proliferation and apoptosis. Compared with adjacent normal tissues, the expression of E-cadherin in human cutaneous melanoma tissues was significantly decreased, whereas the expression of CXCL8, JAK2, STAT3, vimentin and N-cadherin was significantly increased (P<0.05). Compared with the blank group, CXCL8 siRNA group and CXCL8 siRNA + AG490 group had significantly lower expression of CXCL8 (P<0.05). Compared with the blank group, the expression levels of JAK2, STAT3, vimentin and N-cadherin in CXCL8 siRNA group, AG490 group and CXCL8 siRNA + AG490 group were decreased, the expression of E-cadherin was increased, the cell proliferation ability was decreased and apoptosis was increased (P<0.05). Compared with CXCL8 siRNA group, the expression of JAK2, STAT3, vimentin and N-cadherin in CXCL8 siRNA + AG490 group were significantly decreased, the expression of E-cadherin was significantly increased, cell proliferation ability was decreased and apoptosis was increased (P<0.05). In conclusion, CXCL8 gene expression silencing may inhibit EMT and cell proliferation while promoting cell apoptosis of human cutaneous melanoma cells by inhibiting the activation of JAK-STAT signaling pathway.

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From crosslinking strategies to biomedical applications of hyaluronic acid-based hydrogels: A review

Luo

Tan

Zhou

et al. 2023

International Journal of Biological Macromolecules

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Rebooting the collagen gel: Artificial hydrogels for the study of epithelial mesenchymal transformation

Cited by 5 publications

References 57 publications

Adhesion to type I collagen fibrous gels induces E- to N-cadherin switching without other EMT-related phenotypes in lung carcinoma cell A549

Adhesion to type I collagen fibrous gels induces E- to N-cadherin switching without other EMT-related phenotypes in lung carcinoma cell A549

Mechanisms of JAK‑STAT signaling pathway mediated by CXCL8 gene silencing on epithelial‑mesenchymal transition of human cutaneous melanoma cells

From crosslinking strategies to biomedical applications of hyaluronic acid-based hydrogels: A review

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