In Vitro Methods to Study the Modulation of Migration and Invasion by Sphingosine-1-Phosphate

Castro, Melina Gabriela; Campos, Ludmila Estefanía; Rodríguez, Yamila Isabel; Alvarez, Sergio E.

doi:10.1007/7651_2017_51

Cited by 8 publications

(7 citation statements)

References 14 publications

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“…Cell migration is a dynamic process dependent on the presence of a chemoattractant gradient implying cytoskeletal reorganization and formation of structures that enable cell movement [ 26 ]. Despite having similar requirements than migration, invasion, one of the hallmarks of cancer, also involves proteolytic degradation of ECM by MMPs, allowing cancer cells to spread out of the primary tumor [ 36 ].…”

Section: Discussionmentioning

confidence: 99%

“…Cell migration was performed as described previously [ 25 , 26 ]. Briefly, B16.F1 cells were deprived of fetal bovine serum (FBS) for 18 h. MoCM and CM were added to the lower wells of a modified Boyden Chamber and covered with a 12 μm filter previously coated with 10 μg/mL fibronectin.…”

Section: Methodsmentioning

confidence: 99%

“…Equal amount of proteins (70 μg) were subjected to sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) under non-reducing conditions. The gels were copolymerized with 1.5% as previously indicated [ 26 ]. Two gels were run at once and after SDS removal, both gels were incubated for 42 h at 37 °C with gentle shaking.…”

Section: Methodsmentioning

confidence: 99%

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Tumor Necrosis Factor Receptor-1 (p55) Deficiency Attenuates Tumor Growth and Intratumoral Angiogenesis and Stimulates CD8+ T Cell Function in Melanoma

Rodríguez

Campos

Castro

et al. 2020

Cells

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The role of tumor necrosis factor-α (TNF-α) in shaping the tumor microenvironment is ambiguous. Consistent with its uncertain role in melanoma, TNF-α plays a dual role, either acting as a cytotoxic cytokine or favoring a tumorigenic inflammatory microenvironment. TNF-α signals via two cognate receptors, namely TNFR1 (p55) and TNFR2 (p75), which mediate divergent biological activities. Here, we analyzed the impact of TNFR1 deficiency in tumor progression in the B16.F1 melanoma model. Tumors developed in mice lacking TNFR1 (TNFR1 knock-out; KO) were smaller and displayed lower proliferation compared to their wild type (WT) counterpart. Moreover, TNFR1 KO mice showed reduced tumor angiogenesis. Although no evidence of spontaneous metastases was observed, conditioned media obtained from TNFR1 KO tumors increased tumor cell migration. Whereas the analysis of tumor-associated immune cell infiltrates showed similar frequency of total and M2-polarized tumor-associated macrophages (TAMs), the percentage of CD8+ T cells was augmented in TNFR1 KO tumors. Indeed, functional ex vivo assays demonstrated that CD8+ T cells obtained from TNFR1KO mice displayed an increased cytotoxic function. Thus, lack of TNFR1 attenuates melanoma growth by modulating tumor cell proliferation, migration, angiogenesis and CD8+ T cell accumulation and activation, suggesting that interruption of TNF-TNFR1 signaling may contribute to control tumor burden.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Tumor Necrosis Factor Receptor-1 (p55) Deficiency Attenuates Tumor Growth and Intratumoral Angiogenesis and Stimulates CD8+ T Cell Function in Melanoma

Rodríguez

Campos

Castro

et al. 2020

Cells

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“…Wound healing assay was performed as described previously (Castro et al, 2018 ). Migratory capacity of cells was determined by wound healing assay.…”

Section: Methodsmentioning

confidence: 99%

Bisecting N-Acetylglucosamine Structures Inhibit Hypoxia-Induced Epithelial-Mesenchymal Transition in Breast Cancer Cells

Tan

Wang

et al. 2018

Front. Physiol.

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The epithelial-mesenchymal transition (EMT) process plays a key role in many biological processes, including tissue fibrosis, metastatic diseases, and cancer progression. EMT can be induced by certain factors, notably hypoxia, in the tumor microenvironment. Aberrant levels of certain N-glycans is associated with cancer progression. We used an integrated strategy (mass spectrometry in combination with lectin microarray analysis) to elucidate aberrant glycosylation in a hypoxia-induced EMT model using breast cancer cell lines MCF7 and MDA-MB-231. The model showed reduced levels of bisecting GlcNAc structures, and downregulated expression of the corresponding glycosyltransferase MGAT3. MGAT3 overexpression in MCF7 suppressed cell migration, proliferation, colony formation, expression of EMT markers, and AKT signaling pathway, whereas MGAT3 knockdown (shRNA silencing) had opposite effects. Our findings clearly demonstrate the functional role (and effects of dysregulation) of bisecting GlcNAc structures in hypoxia-induced EMT, and provide a useful basis for further detailed studies of physiological functions of these structures in breast cancer.

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“…2D-G, IM + Tan significantly reduced the number of invading cells and the wound closure rate compared with the IM (5 µM) and TIB-152 groups. Extracellular matrix degradation induced by MMPs is required for cell invasion and VEGF plays a key role in mediating cell migration (26,27). Therefore, western blotting was used to analyze the effects of Tan IIA and IM on the expression of VEGF and MMP-9.…”

Section: Tan Iia Enhances the Inhibitory Effect Of Im On Invasion Andmentioning

confidence: 99%

Tanshinone IIA enhances the inhibitory effect of imatinib on proliferation and motility of acute leukemia cell line TIB‑152 in�vivo and in�vitro by inhibiting the PI3K/AKT/mTOR signaling pathway

Teng¹,

Xu²,

Qin³

2019

Oncol Rep

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Acute lymphoblastic leukemia (ALL) is a malignant hematological disease. Tanshinone IIA (Tan IIA) has antitumor activity in vitro and in vivo. The aim of the present study was to investigate the effects of Tan IIA in combination with imatinib (IM) on the proliferation, apoptosis, migration and invasion of acute T lymphocytic leukemia TIB-152 cells in vivo and in vitro, and analyze the potential underlying mechanism. Tan IIA and IM, alone and in combination, significantly inhibited proliferation, migration and invasion of TIB-152 cells, and promoted apoptosis; the effect of co-treatment with Tan IIA plus IM was enhanced. IGF-1 promoted the proliferation, migration and invasion of TIB-152 cells and inhibited apoptosis, while Tan IIA treatment significantly reversed these effects. In vivo experiments demonstrated that treatment with Tan IIA and IM, alone or in combination, significantly inhibited tumor growth in TIB-152 xenograft mice; the growth inhibition of Tan IIA plus IM was the strongest observed. Western blot analysis revealed that the combination of Tan IIA and IM resulted in significantly lower levels of p-PI3K, p-AKT and p-mTOR in cells and tissues compared with the IM and Tan alone treatment groups. In addition, the combination of Tan IIA and IM significantly decreased the levels of Ki67, cleaved caspase-3, VEGF and MMP-9 in cells and tissues, and the level of caspase-3 was significantly increased. Taken together, the results revealed that Tan IIA enhanced the inhibitory effect of imatinib on TIB-152 cell proliferation, migration and invasion, and induced apoptosis, which may be associated with inhibition of the PI3K/AKT/mTOR signaling pathway. Tanshinone IIA enhances the inhibitory effect of imatinib on proliferation and motility of acute leukemia cell line TIB-152 in vivo and in vitro by inhibiting the PI3K/AKT/mTOR signaling pathway

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In Vitro Methods to Study the Modulation of Migration and Invasion by Sphingosine-1-Phosphate

Cited by 8 publications

References 14 publications

Tumor Necrosis Factor Receptor-1 (p55) Deficiency Attenuates Tumor Growth and Intratumoral Angiogenesis and Stimulates CD8+ T Cell Function in Melanoma

Tumor Necrosis Factor Receptor-1 (p55) Deficiency Attenuates Tumor Growth and Intratumoral Angiogenesis and Stimulates CD8+ T Cell Function in Melanoma

Bisecting N-Acetylglucosamine Structures Inhibit Hypoxia-Induced Epithelial-Mesenchymal Transition in Breast Cancer Cells

Tanshinone IIA enhances the inhibitory effect of imatinib on proliferation and motility of acute leukemia cell line TIB‑152 in�vivo and in�vitro by inhibiting the PI3K/AKT/mTOR signaling pathway

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