Mechanisms of RON-mediated epithelial-mesenchymal transition in MDCK cells through the MAPK pathway

Xu, Xiao; Qian, Yun; Zhang, Guoliang; Lin, Jie

doi:10.1590/s0100-879x2011007500070

Cited by 12 publications

(13 citation statements)

References 24 publications

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“…Through stable-transfection of MGC-803 cells with a variant RONΔ160 expressing plasmid, the overexpression of RONΔ160 in gastric cancer cells was successfully simulated. The observed change in the shape of RONΔ160 overexpressing MGC-803 cells from the previous flat circular shape or polygon to a spindle is similar to the result of Xu et al [ 18 ], which confirmed that overexpression of RON changes the original shape of MDCK cells. The change of cell shape is likely related to RONΔ160-mediated epithelial-mesenchymal transition (EMT), i.e.…”

Section: Discussionsupporting

confidence: 87%

Variant RONΔ160 of the RON receptor tyrosine kinase promotes the growth and invasion in vitro and in vivo in gastric cancer cell lines

Zhou

Yang

2015

Cancer Cell International

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BackgroundRecepteur d’origine nantais (RON) is a receptor tyrosine kinase whose overexpression has been observed in human gastric cancers. This study aimed to determine whether overexpression of the variant RONΔ160 could induce tumorigenicity of gastric cancer cells in vitro or in vivo, and whether its specific small molecule inhibitor (Compound I) could inhibit the effect of RONΔ160.MethodsWe constructed human gastric cancer cell line MGC-803 that was stably transfected with a recombinant plasmid expressing RONΔ160, and the effect of RONΔ160 overexpression and macrophage-stimulating protein (MSP) activation on proliferation, migration and invasion abilities of MGC-803 cells were evaluated. Tumor-bearing mice with gastric cancer cells were used to analyze the effects of RONΔ160 overexpression and Compound I on implanted tumor growth.ResultsIn vitro, overexpression of RONΔ160 in MGC-803 cells resulted changes to their cell morphology, and promoted cell proliferation, migration and invasion. In addition, overexpression of RONΔ160 increased the proportion of cells in the S phase. The effect of RONΔ160 was significantly enhanced by induction of MSP inducing (p < 0.05). In vivo, RONΔ160 promoted the growth of MGC-803 cells in nude mice, including increased tumor size and weight, and lower tumor incubation period. The Compound I inhibited the tumorigenic abilities of RONΔ160 (p <0.05).ConclusionsThe results indicate that overexpression of the variant RONΔ160 altered the phenotype and tumorigenicity of MGC-803 cells. Its specific small molecule inhibitor could inhibit the effect of RONΔ160. Therefore, the variant RONΔ160 may become a potential therapeutic target for gastric cancer.

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Section: Discussionsupporting

confidence: 87%

Variant RONΔ160 of the RON receptor tyrosine kinase promotes the growth and invasion in vitro and in vivo in gastric cancer cell lines

Zhou

Yang

2015

Cancer Cell International

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“…In human cancer, activation of PI3K/Akt with downregulation of E-cadherin expression and induction of EMT may be particularly important. 26, 27, 28, 29 GSK-3 β is a multifunctional serine/threonine (ser/thr) kinase that has a fundamental role in a wide variety of functions, including cell division, proliferation, differentiation and adhesion. 30, 31, 32 GSK-3 β is active in resting epithelial cells, and inhibition of its activity or its expression may lead to EMT.…”

Section: Resultsmentioning

confidence: 99%

Role of fucosyltransferase IV in epithelial–mesenchymal transition in breast cancer cells

2013

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Epithelial–mesenchymal transition (EMT) is a crucial step in tumor progression and has an important role during cancer invasion and metastasis. Although fucosyltransferase IV (FUT4) has been implicated in the modulation of cell migration, invasion and cancer metastasis, its role during EMT is unclear. This study explores the molecular mechanisms of the involvement of FUT4 in EMT in breast cancer cells. Breast cancer cell lines display increased expression of FUT4, which is accompanied by enhanced appearance of the mesenchymal phenotype and which can be reversed by knockdown of endogenous FUT4. Moreover, FUT4 induced activation of phosphatidylinositol 3-kinase (PI3K)/Akt, and inactivation of GSK3β and nuclear translocation of NF-κB, resulting in increased Snail and MMP-9 expression and greater cell motility. Taken together, these findings indicate that FUT4 has a role in EMT through activation of the PI3K/Akt and NF-κB signaling systems, which induce the key mediators Snail and MMP-9 and facilitate the acquisition of a mesenchymal phenotype. Our findings support the possibility that FUT4 is a novel regulator of EMT in breast cancer cells and a promising target for cancer therapy.

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“…Dissociation was followed by nuclear accumulation of RSK2 and the subsequent increase in EMT markers such as decreased E-cadherin and increased vimentin [39]. Others confirmed these results with regard to Ron and EMT, where HGFL stimulation of MDCK cells stably expressing Ron leads to loss of epithelial markers and increased mesenchymal markers through a similar pathway [40]. …”

Section: Ron and Cancermentioning

confidence: 94%

Ron receptor tyrosine kinase signaling as a therapeutic target

Benight

Waltz

2012

Expert Opinion on Therapeutic Targets

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Mechanisms of RON-mediated epithelial-mesenchymal transition in MDCK cells through the MAPK pathway

Cited by 12 publications

References 24 publications

Variant RONΔ160 of the RON receptor tyrosine kinase promotes the growth and invasion in vitro and in vivo in gastric cancer cell lines

Variant RONΔ160 of the RON receptor tyrosine kinase promotes the growth and invasion in vitro and in vivo in gastric cancer cell lines

Role of fucosyltransferase IV in epithelial–mesenchymal transition in breast cancer cells

Ron receptor tyrosine kinase signaling as a therapeutic target

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