Probing the Adhesion of Hepatocellular Carcinoma HepG2 and SK‐Hep‐1 Cells

Hsieh, Shuchen; Lin, Pei‐Ying; Hsieh, Chiung-Wen; Li, I-Tin; Hsieh, Shu‐Ling; Wu, Chih-Chung; Huang, Yun-Shan; Wang, Huay-Min; Tu, Li‐Wei; Cheng, Kuang‐Hung; Wang, Hay-Yan Jack; Wu, Deng‐Chyang

doi:10.1002/jccs.201200129

Cited by 6 publications

(3 citation statements)

References 19 publications

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“…We further investigated whether the expression of SPHK1 promotes the invasion and metastasis of HCC cells by regulating the EMT. Because both the expression of SPHK1 6 and mobility 13 of HepG2 cells are lower than those of other HCC cells, we prepared HepG2 cells stably expressing either vector or MYC-SPHK1. The data showed that the overexpression of SPHK1 resulted in enhanced migration, as indicated by transwell migratory assay, as well as increased invasion, as indicated by Martrigel invasion assay ( Fig.…”

Section: Resultsmentioning

confidence: 99%

SPHK1 (sphingosine kinase 1) induces epithelial-mesenchymal transition by promoting the autophagy-linked lysosomal degradation of CDH1/E-cadherin in hepatoma cells

Liu

et al. 2017

Autophagy

113

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SPHK1 (sphingosine kinase 1), a regulator of sphingolipid metabolites, plays a causal role in the development of hepatocellular carcinoma (HCC) through augmenting HCC invasion and metastasis. However, the mechanism by which SPHK1 signaling promotes invasion and metastasis in HCC remains to be clarified. Here, we reported that SPHK1 induced the epithelial-mesenchymal transition (EMT) by accelerating CDH1/E-cadherin lysosomal degradation and facilitating the invasion and metastasis of HepG2 cells. Initially, we found that SPHK1 promoted cell migration and invasion and induced the EMT process through decreasing the expression of CDH1, which is an epithelial marker. Furthermore, SPHK1 accelerated the lysosomal degradation of CDH1 to induce EMT, which depended on TRAF2 (TNF receptor associated factor 2)-mediated macroautophagy/autophagy activation. In addition, the inhibition of autophagy recovered CDH1 expression and reduced cell migration and invasion through delaying the degradation of CDH1 in SPHK1-overexpressing cells. Moreover, the overexpression of SPHK1 produced intracellular sphingosine-1-phosphate (S1P). In response to S1P stimulation, TRAF2 bound to BECN1/Beclin 1 and catalyzed the lysine 63-linked ubiquitination of BECN1 for triggering autophagy. The deletion of the RING domain of TRAF2 inhibited autophagy and the interaction of BECN1 and TRAF2. Our findings define a novel mechanism responsible for the regulation of the EMT via SPHK1-TRAF2-BECN1-CDH1 signal cascades in HCC cells. Our work indicates that the blockage of SPHK1 activity to attenuate autophagy may be a promising strategy for the prevention and treatment of HCC.

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Section: Resultsmentioning

confidence: 99%

SPHK1 (sphingosine kinase 1) induces epithelial-mesenchymal transition by promoting the autophagy-linked lysosomal degradation of CDH1/E-cadherin in hepatoma cells

Liu

et al. 2017

Autophagy

113

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“…Multiple curves were acquired (997–1024) for each sample and analyzed using the data analysis tools built into the AFM software (Igor pro 6.37). A detailed description of the force curve analysis and Young's modulus calculation is described in our previous work [ 39 , 40 ]. All Raman experiments were performed on a Raman microscope (WiTec alpha 300R) with a 532 nm incident laser at 15 mW power.…”

Section: Methodsmentioning

confidence: 99%

Surface degradation effects of carbonated soft drink on a resin based dental compound

Tseng

Lin

Kirankumar

et al. 2021

Heliyon

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Dental compounds and restorative materials undergo surface degradation and erosion from exposure to a variety of dietary substances. In this study we investigated changes in the surface properties of Rebaron, a hard denture reline material (HDRM), following timed immersion in carbonated soft drinks to determine its durability in a common acidic environment. Samples were prepared and immersed in a carbonated soft drink (or its components) for 6, 12, or 24 h. Surface structure and mechanical properties were characterized using Atomic Force Microscopy (AFM). Raman spectroscopy was used to identify changes in the HDRM surface chemistry following exposure to the test solutions. AFM revealed that prolonged exposure led to pit formation and a subsequent increase in surface roughness, from 302.02 ± 30.20 to 430.59 ± 15.07 nm Ra, following a 24 h exposure. Young's modulus values decreased from 9.3 ± 7.0 to 0.53 ± 0.26 GPa under the same conditions, demonstrating a softening and embrittlement of the HDRM sample. Raman results revealed that immersion in the carbonated soft drink or acidic solution changed the nature of the HDRM structure, converting the HDRM surface chemistry from primarily hydrophobic to hydrophilic. Our study indicates that sustainability and durability of Rebaron HDRM are significantly reduced by prolonged exposure to carbonated (acidic) soft drink, resulting in deformation and degradation of the material surface.

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“…Our findings were similar to those of a recent study [29], in which 3D cultured HepG2 cells quickly clustered and proliferated, followed by sharp decline from day 7 when assayed by immunostaining against the proliferation marker Ki67. The decreased proliferation was assumed to be due to contact inhibition since studies reported that HepG2 cells usually grow in aggregates in 3D environment [30]. Moreover, albumin and urea secretion of HepG2 cells were assayed, and the results showed that HepG2 cells increased the secretions over the time first and then decreased on day 7, which was consistent with the cell proliferation trend (figures 3(E) and (F)), suggesting that the highly proliferating HepG2 cells held the typical hepatic property in the 3D hepatic structure.…”

Section: Biocompatibility Available and Valid Perfusion Of The Double...mentioning

confidence: 99%

Dual-core coaxial bioprinting of double-channel constructs with a potential for perfusion and interaction of cells

Yu¹,

Xie²,

He³

et al. 2022

Biofabrication

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Coaxial bioprinting of hydrogel tubes has tremendous potential in the fabrication of highly complex large-scale vascularized structures, however, constructs with bioinks of simultaneous weak printability and perfusable networks have not been reported. Here, we report a coaxial printing method in which double-channel filaments are three-dimensional (3D) extrusion-bioprinted using a customized dual-core coaxial nozzle. The filament in one channel can perform core/shell role and the other channel can play a role in perfusion. These parallel channels within filaments are separated by an interval wall of alginate, whose thickness (∼50 μm) is beneficial to supplement nutrients via perfusion. Different cell-laden hydrogels of weak mechanics were used to test the adaptability and perfusability of our method, and the results showed that dynamic perfusion maintained higher viability and functions than static culture. By combining with a bioprinter, 8-layer perfusable double-channel constructs were fabricated, and the cell viabilities gradually decreased with the reduction in nutrients and oxygen in the downstream medium. Furthermore, the double-channel filaments were tested as a platform to mimic dynamic functions between cells through sequential perfusion by using Mouse insulinoma 6 (Min6) and Hepatocellular carcinoma (HepG2) as the model cells. These results demonstrated the insulin secreted by Min6 upstream simulated and increased the uptake of glucose by the downstream HepG2 cells. In conclusion, our study provided evidence for the probability of all-in-one fabrication of 3D double-channel perfusable constructs with high simplicity, expansibility, and versability. Our strategy has significant potential for building large-scale tissue constructs for applications in tissue engineering, possibly even in drug screening and regenerative medicine.

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Probing the Adhesion of Hepatocellular Carcinoma HepG2 and SK‐Hep‐1 Cells

Cited by 6 publications

References 19 publications

SPHK1 (sphingosine kinase 1) induces epithelial-mesenchymal transition by promoting the autophagy-linked lysosomal degradation of CDH1/E-cadherin in hepatoma cells

SPHK1 (sphingosine kinase 1) induces epithelial-mesenchymal transition by promoting the autophagy-linked lysosomal degradation of CDH1/E-cadherin in hepatoma cells

Surface degradation effects of carbonated soft drink on a resin based dental compound

Dual-core coaxial bioprinting of double-channel constructs with a potential for perfusion and interaction of cells

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