E-cadherin-dependent intercellular adhesion enhances chemoresistance

Nakamura, Tomoaki; Kato, Yasushi; Fuji, Hidenori; Horiuchi, Tetsuya; Chiba, Yukio; Tanaka, Kuniyoshi

doi:10.3892/ijmm.12.5.693

Cited by 51 publications

(70 citation statements)

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“…In regard to the relationship between irradiation and EMT, Andarawewa et al reported that irradiation induced TGF-β-mediated EMT (24). Several studies have examined the possible role of EMT in CRC progression (25,26), and the association between chemoresistance and EMT in CRC (27)(28)(29). On the other hand, Kumar et al (12,13) and Speake et al (14) and described that irradiation enhanced the migration and invasiveness of CRC cells in association with enhanced expression and activity of MMPs, but no studies have referred to radiation-induced EMT in CRC cells.…”

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confidence: 99%

Radiation induces epithelial-mesenchymal transition in colorectal cancer cells

Kawamoto

Yokoe²,

Tanaka³

et al. 2011

Oncol Rep

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Abstract. Radiotherapy remains a major approach to adjuvant therapy for patients with advanced rectal cancer. Nevertheless, the effects of radiation on malignant processes have yet to be clarified. The aim of this study was to assess the biological effects of radiation on colorectal cancer (CRC) cells with special reference to epithelial-mesenchymal transition (EMT), a key developmental program often activated during cancer invasion and metastasis. We investigated the effect of radiation on two colorectal cancer cell lines, CaR1 and DLD1, assessing cell morphology, motility, migration and invasive ability. Expression of molecules associated with EMT was determined using RT-PCR, Western blotting, and immunofluorescence staining in control and irradiated cells. We also used real-time RT-PCR to examine the expression of molecules associated with EMT before and after chemoradiotherapy. Thus, we studied 26 rectal cancer patients who received preoperative chemoradiotherapy followed by radical surgery. In addition, we examined the relationship between disease recurrence and the expression of a number of proteins. Irradiation caused CRC cells to undergo phenotypic changes characteristic of EMT: spindle-cell shape, loss of polarity, intercellular separation and pseudopodia formation. Irradiation enhanced cell migration and invasiveness. In irradiated CRC cells, molecular changes consistent with EMT were observed. In clinical samples, we observed molecular changes consistent with EMT, and those changes were significantly enhanced in patients with recurring disease. These results indicate that irradiation induces an alteration to a malignant phenotype consistent with EMT in colorectal cancer cells.

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confidence: 99%

Radiation induces epithelial-mesenchymal transition in colorectal cancer cells

Kawamoto

Yokoe²,

Tanaka³

et al. 2011

Oncol Rep

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“…[12][13][14][15][16][17] Several lines of evidence suggest that the vascular cell adhesion and signaling receptor, PECAM-1, may be one such molecule. PECAM-1 is a homophilic binding member of the immunoglobulin gene/immunoreceptor tyrosine-based inhibitory motif (Ig-ITIM) family of inhibitory receptors 18 that is expressed on most human CD34 + hematopoietic progenitor cells, 19 well as on myeloid and megakaryocytic lineages, subsets of B and T lymphocytes, and at endothelial cell-cell junctions.…”

Section: Introductionmentioning

confidence: 99%

The cell-adhesion and signaling molecule PECAM-1 is a molecular mediator of resistance to genotoxic chemotherapy

Bergom¹,

Goel²,

Paddock³

et al. 2006

Cancer Biology & Therapy

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“…Moreover, in addition to interacting with Mig-2 [5] , the C-terminal LIM domains have been implicated in the localization of migfilin to cell-cell adhesions through regulation of the cadherin-β-catenin complex [4,16] . Previous studies have reported that the regulation of cell-cell junctions by E-cadherin could influence cisplatin-based chemoresistance [19][20][21] . In human glioma cells, expression levels of E-cadherin, β-catenin and PARP are regulated in ZEB2-mediated cellular apoptosis [22] .…”

Section: Discussionmentioning

confidence: 99%

Migfilin sensitizes cisplatin-induced apoptosis in human glioma cells in vitro

Fan

et al. 2012

Acta Pharmacol Sin

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Aim: Filamin binding LIM protein 1, also known as migfilin, is a skeleton organization protein that binds to mitogen-inducible gene 2 at cell-extracellular matrix adhesions. The aim of this study was to investigate the role of migfilin in cisplatin-induced apoptosis in human glioma cells, to determine the functional domains of migfilin, and to elucidate the molecular mechanisms underlying the regulation of cisplatin-related chemosensitivity. Methods: The human glioma cell lines Hs683, H4, and U-87 MG were transfected with pEGFP-C2-migfilin to elevate the expression level of migfilin. RNA interference was used to reduce the expression of migfilin. To determine the functional domains of migfilin, U-87 MG cells were transfected with plasmids of migfilin deletion mutants. After treatment with cisplatin (40 µmol/L) for 24 h, the cell viability was assessed using the MTS assay, and the cell apoptotic was examined using the DAPI staining assay and TUNEL analysis. Expression levels of apoptosis-related proteins were detected by Western blot analysis. Results: Overexpression of migfilin significantly enhanced cisplatin-induced apoptosis in Hs683, H4, and U-87 MG cells, whereas downregulation of migfilin expression inhibited the chemosensitivity of these cell lines. The N-terminal region of migfilin alone was able to enhance the cisplatin-induced apoptosis. However, despite the existence of the N-terminal region, mutants of migfilin with any one of three LIM domains deleted led to a function loss. Furthermore, apoptotic proteins (PARP and caspase-3) and the anti-apoptotic protein Bcl-xL were modulated by the expression level of migfilin in combination with cisplatin. Conclusion: The LIM1-3 domains of migfilin play a key role in sensitizing glioma cells to cisplatin-induced apoptosis through regulation of apoptosis-related proteins.

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E-cadherin-dependent intercellular adhesion enhances chemoresistance

Cited by 51 publications

References 0 publications

Radiation induces epithelial-mesenchymal transition in colorectal cancer cells

Radiation induces epithelial-mesenchymal transition in colorectal cancer cells

The cell-adhesion and signaling molecule PECAM-1 is a molecular mediator of resistance to genotoxic chemotherapy

Migfilin sensitizes cisplatin-induced apoptosis in human glioma cells in vitro

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