Journal: International journal of molecular sciences

Article Title: Preconditioned Chorionic Villus Mesenchymal Stem/Stromal Cells (CVMSCs) Minimize the Invasive Phenotypes of Breast Cancer Cell Line MDA231 In Vitro.

doi: 10.3390/ijms24119569

Figure Lengend Snippet: Figure 6. Modulation in expression of tumor suppressor proteins and oncogenes in MDA231 cells treated with preconditioned CVMSCs: flow cytometry analysis for the expression of tumor suppressor proteins modulated in MDA231 cells after treatment with preconditioned CVMSCs showed significant increase in the expression levels for CDH1 and IFN-gamma in both IC and CM settings as compared to untreated control (A(i)). Expression levels of oncogenes such as IDO, IL6, MMP7, and TGF-β1 reduced significantly in MDA231 cells in both IC and SF setting as compared to untreated control (B(i)). Data obtained by FACS analysis from three independent experiments were quantified and are shown in bar graphs as Mean Florescence Index (MFI) pertaining to CDH1 and IFN-gamma (A(ii)), and IDO, IL6, MMP7, and TGF-β1 (B(ii)), respectively. Bars represent standard errors. * p < 0.05.

Article Snippet: Fluorescent-labeled antibodies for flow cytometry experiments, including IFN-γ (Human IFN-gamma PE-conjugated Antibody) cat# IC285P; CDH1 (Human E-Cadherin PE-conjugated Antibody) cat# FAB18381P; IDO (Human Indoleamine 2,3-dioxygenase/IDO PE-conjugated Antibody) cat# IC6030P; IL6 (Human IL-6 PE-conjugated Antibody)cat# IC206P; MMP7 (Human MMP-7 PE-conjugated Antibody) cat# IC9071P; and TGF-β1 (Human TGF-beta 1 Alexa Fluor® 488-conjugated Antibody) cat# IC10502G were purchased from R&D Systems (Minneapolis, MN, USA).

Techniques: Expressing, Cytometry, Control

Journal: The Journal of Neuroscience

Article Title: MPP3 Is Required for Maintenance of the Apical Junctional Complex, Neuronal Migration, and Stratification in the Developing Cortex

doi: 10.1523/JNEUROSCI.5627-12.2013

Figure Lengend Snippet: Disruption of adherens junctions in Mpp3 cKO cortex. A–C, p120 catenin levels and apical membrane localization are essentially unaffected in E12.5 Mpp3 cKO cortex. At areas with a loss of p120 catenin, there is cellular disorganization in the ventricular zone (C). B and C are magnification of boxes 1 and 2 in A, respectively. D, E, Likewise, at areas in which Nectin1 is unaffected, cellular organization is indistinguishable from control cortex, but at areas with a loss of Nectin1, a clear disruption of cellular organization was observed (E). F, G, No difference in level and localization of adherens junction protein β-catenin between control (F) and Mpp3 cKO (G) at the level of the third ventricle in which Cre recombinase is not expressed. H, I, Whereas β-catenin displays a punctate pattern at the apical membrane in control cortex (H), in the Mpp3 cKO, there is a loss and delocalization of β-catenin (I). J–O, The same differences were observed between control and Mpp3 cKO for adherens junction proteins p120 catenin (J, K), N-cadherin (L, M), and M-cadherin (N, O). P, Q, Clear loss of Nectin1, which directly interacts with MPP3, during loss of MPP3. R, S, The PAR complex member PAR3 has a punctate distribution in the control cortex (R), but in the Mpp3 cKO cortex, there is a prominent loss of PAR3 from the apical membrane (S). Scale bars, 20 μm.

Article Snippet: Le Bivic, Developmental Biology Institute of Marseille Luminy, Marseille, France), Nectin1 (1:500; MBL), β-catenin (1:100; BD Biosciences), p120 catenin (1:100; BD Biosciences), N-cadherin (1:500; BD Biosciences), M-cadherin (1:500; BD Biosciences), PAR3 (1:200; Millipore), phospho-Histone H3 (pH3; 1:500; Millipore), BrdU (1:250, Abcam), Ki67 (1:100; BD Biosciences), CUX1 (1:200; Santa Cruz Biotechnology), CTIP2 (1:100; Abcam), Calretinin (1:500; Millipore Bioscience Research Reagents), Sox2 (1:300; Millipore Bioscience Research Reagents), Tbr1 (1:200; Abcam), Tbr2 (1:200; Abcam), and Tuj1 (1:200; Covance).

Techniques:

Journal: International Journal of Oncology

Article Title: Sphingosine kinase 1 promotes the metastasis of colorectal cancer by inducing the epithelial-mesenchymal transition mediated by the FAK/AKT/MMPs axis

doi: 10.3892/ijo.2018.4607

Figure Lengend Snippet: Expression of SphK1, FAK, p-FAK, E-cadherin and vimentin in colorectal cancer. (A) Immunohistochemical staining of SphK1, FAK, p-FAK, E-cadherin and vimentin proteins in normal colonic mucosa tissues, non-metastatic cancer tissues and metastatic cancer tissue samples (magnification, ×100). (B) Survival rate of patients with SphK1-positive and SphK1-negative colorectal cancer. P=0.0169 vs. SphK1-negative. SphK1, Sphingosine kinase 1; FAK, focal adhesion kinase; p, phosphorylated.

Article Snippet: Polyclonal antibodies against E-cadherin (cat. no. bs-1519R; 1:200) and vimentin (cat. no. bs-8533R; 1:200) were from BIOSS (Beijing, China).

Techniques: Expressing, Immunohistochemical staining, Staining

Journal: International Journal of Oncology

Article Title: Sphingosine kinase 1 promotes the metastasis of colorectal cancer by inducing the epithelial-mesenchymal transition mediated by the FAK/AKT/MMPs axis

doi: 10.3892/ijo.2018.4607

Figure Lengend Snippet: Expression of E-cadherin and vimentin in tissues assessed by immunohistochemistry staining.

Article Snippet: Polyclonal antibodies against E-cadherin (cat. no. bs-1519R; 1:200) and vimentin (cat. no. bs-8533R; 1:200) were from BIOSS (Beijing, China).

Techniques: Expressing, Immunohistochemistry, Staining

Journal: International Journal of Oncology

Article Title: Sphingosine kinase 1 promotes the metastasis of colorectal cancer by inducing the epithelial-mesenchymal transition mediated by the FAK/AKT/MMPs axis

doi: 10.3892/ijo.2018.4607

Figure Lengend Snippet: Clinicopathological characteristics of the patients with colorectal cancer and E-cadherin, vimentin expression in the colorectal cancer tissues.

Article Snippet: Polyclonal antibodies against E-cadherin (cat. no. bs-1519R; 1:200) and vimentin (cat. no. bs-8533R; 1:200) were from BIOSS (Beijing, China).

Techniques: Expressing

Journal: Cancer Cell International

Article Title: Circ_ZFR contributes to the paclitaxel resistance and progression of non-small cell lung cancer by upregulating KPNA4 through sponging miR-195-5p

doi: 10.1186/s12935-020-01702-0

Figure Lengend Snippet: Silencing of circ_ZFR inhibited PTX resistance and malignant cell behaviors in PTX-resistant NSCLC cells. Si-circ_ZFR or si-NC was transfected into A549/PTX and H460/PTX cells. a QRT-PCR assay was conducted for circ_ZFR and ZFR expression levels in A549/PTX and H460/PTX cells. b MTT assay was adopted to determine IC 50 of PTX in A549/PTX and H460/PTX cells. c , d Flow cytometry analysis was performed to analyze cell cycle process in A549/PTX and H460/PTX cells. e , f MTT assay was utilized for the detection of cell proliferation in A549/PTX and H460/PTX cells. g Western blot assay was conducted for Ki67 protein level in A549/PTX and H460/PTX cells. h Flow cytometry analysis was used for cell apoptosis ability in A549/PTX and H460/PTX cells. i , j Transwell assay was conducted to examine the migration and invasion of A549/PTX and H460/PTX cells. k , l Western blot assay was conducted for the protein levels of Twist1, E-cadherin and N-cadherin in A549/PTX and H460/PTX cells. * P < 0.05

Article Snippet: The primary antibodies used in this study included Ki67 (bs-23103R; Bioss), Twist1 (bs-2441R; Bioss), E-cadherin (bs-1519R; Bioss), N-cadherin (bs20623R; Bioss) KPNA4 (bs-16804R; Bioss), CyclinD1 (bs-0623R; Bioss), Bcl-2 (bs-33411R; Bioss), Bax (bs-0127R; Bioss) and GAPDH (bs-10900R; Bioss).

Techniques: Transfection, Quantitative RT-PCR, Expressing, MTT Assay, Flow Cytometry, Western Blot, Transwell Assay, Migration

Journal: Cancer Cell International

Article Title: Circ_ZFR contributes to the paclitaxel resistance and progression of non-small cell lung cancer by upregulating KPNA4 through sponging miR-195-5p

doi: 10.1186/s12935-020-01702-0

Figure Lengend Snippet: Circ_ZFR promoted PTX resistance and cell progression in PTX-resistant NSCLC cells by targeting miR-195-5p. A549/PTX and H460/PTX cells were treated with si-NC, si-circ_ZFR, si-circ_ZFR + anti-miR-NC or si-circ_ZFR + anti-miR-195-5p. a QRT-PCR assay was utilized for miR-195-5p level in A549/PTX and H460/PTX cells. b IC 50 of PTX in A549/PTX and H460/PTX cells was estimated by MTT assay. c – f Cell cycle and cell proliferation in A549/PTX and H460/PTX cells were analyzed by flow cytometry analysis and MTT assay, respectively. g Western blot assay was conducted for Ki67 protein level in A549/PTX and H460/PTX cells. h Cell apoptosis, i , j migration and invasion in A549/PTX and H460/PTX cells were assessed by flow cytometry analysis and transwell assay, respectively. k , l The protein levels of Twist1, E-cadherin and N-cadherin in A549/PTX and H460/PTX cells were measured through western blot assay. * P < 0.05

Article Snippet: The primary antibodies used in this study included Ki67 (bs-23103R; Bioss), Twist1 (bs-2441R; Bioss), E-cadherin (bs-1519R; Bioss), N-cadherin (bs20623R; Bioss) KPNA4 (bs-16804R; Bioss), CyclinD1 (bs-0623R; Bioss), Bcl-2 (bs-33411R; Bioss), Bax (bs-0127R; Bioss) and GAPDH (bs-10900R; Bioss).

Techniques: Quantitative RT-PCR, MTT Assay, Flow Cytometry, Western Blot, Migration, Transwell Assay

Journal: Cancer Cell International

Article Title: Circ_ZFR contributes to the paclitaxel resistance and progression of non-small cell lung cancer by upregulating KPNA4 through sponging miR-195-5p

doi: 10.1186/s12935-020-01702-0

Figure Lengend Snippet: MiR-195-5p overexpression suppressed PTX resistance and malignant behaviors of PTX-resistant NSCLC cells by binding to KPNA4. A549/PTX and H460/PTX cells were assigned to miR-195-5p, miR-NC, miR-195-5p + KPNA4 and miR-195-5p + pcDNA groups. a , b The mRNA and protein levels of KPNA4 in A549/PTX and H460/PTX cells were determined by qRT-PCR assay and western blot assay, respectively. c IC 50 of PTX in A549/PTX and H460/PTX cells was evaluated using MTT assay. d – g Cell cycle and cell proliferation in A549/PTX and H460/PTX cells were estimated using flow cytometry analysis and MTT assay, respectively. h The protein level of Ki67 in A549/PTX and H460/PTX cells was measured using western blot assay. i Cell apoptosis, j , k migration and invasion in A549/PTX and H460/PTX cells were analyzed by flow cytometry analysis and transwell assay, respectively. l , m The protein levels of Twist1, E-cadherin and N-cadherin in A549/PTX and H460/PTX cells were measured by western blot assay. * P < 0.05

Article Snippet: The primary antibodies used in this study included Ki67 (bs-23103R; Bioss), Twist1 (bs-2441R; Bioss), E-cadherin (bs-1519R; Bioss), N-cadherin (bs20623R; Bioss) KPNA4 (bs-16804R; Bioss), CyclinD1 (bs-0623R; Bioss), Bcl-2 (bs-33411R; Bioss), Bax (bs-0127R; Bioss) and GAPDH (bs-10900R; Bioss).

Techniques: Over Expression, Binding Assay, Quantitative RT-PCR, Western Blot, MTT Assay, Flow Cytometry, Migration, Transwell Assay

Journal: Journal of Translational Medicine

Article Title: Development of patient-derived xenograft models from a spontaneously immortal low-grade meningioma cell line, KCI-MENG1

doi: 10.1186/s12967-015-0596-8

Figure Lengend Snippet: Immunostaining of original tumor, low passage, and high passage KCI-MENG1 cells. The original patient-derived tumor ( top row ) showed moderate and patchy immunoreactivity for epithelial membrane antigen (EMA); strong and diffuse immunostaining for progesterone receptor (PR); and a Ki-67 proliferative index of 2–3%. There was also strong immunostaining for N-cadherin and vimentin. KCI-MENG1-LP cells ( middle row ) and KCI-MENG1-HP cells ( bottom row ) maintained expression of EMA, N-cadherin, and vimentin but had significantly reduced PR expression compared to the original tumor. Whereas Ki-67 labeling was found in only a small number of cells in the original tumor and low passage cells, it was positive in virtually all P84 cells. Scale bar 50 µm.

Article Snippet: Primary antibodies used targeted the following proteins: EMA (cat.#247M-94), PR (cat.#323R-14), Ki-67 (cat.#275R-14), vimentin (cat.#347R-14; all from CellMarque, Rocklin, CA, USA), and N-cadherin (cat.#NBP1-48309, Novus Biologicals, Littleton, CO, USA).

Techniques: Immunostaining, Derivative Assay, Membrane, Expressing, Labeling

Journal: Journal of Translational Medicine

Article Title: Development of patient-derived xenograft models from a spontaneously immortal low-grade meningioma cell line, KCI-MENG1

doi: 10.1186/s12967-015-0596-8

Figure Lengend Snippet: Immunostaining of original patient tumor, low and high passage KCI-MENG1 cells, and subcutaneous xenograft tumor. The original patient-derived tumor showed moderate immunoreactivity for E-cadherin which was maintained in all in vitro and in vivo models. Scale bar 50 µm.

Article Snippet: Primary antibodies used targeted the following proteins: EMA (cat.#247M-94), PR (cat.#323R-14), Ki-67 (cat.#275R-14), vimentin (cat.#347R-14; all from CellMarque, Rocklin, CA, USA), and N-cadherin (cat.#NBP1-48309, Novus Biologicals, Littleton, CO, USA).

Techniques: Immunostaining, Derivative Assay, In Vitro, In Vivo

Journal: Journal of Translational Medicine

Article Title: Development of patient-derived xenograft models from a spontaneously immortal low-grade meningioma cell line, KCI-MENG1

doi: 10.1186/s12967-015-0596-8

Figure Lengend Snippet: Meningioma cell lines reported in the literature

Article Snippet: Primary antibodies used targeted the following proteins: EMA (cat.#247M-94), PR (cat.#323R-14), Ki-67 (cat.#275R-14), vimentin (cat.#347R-14; all from CellMarque, Rocklin, CA, USA), and N-cadherin (cat.#NBP1-48309, Novus Biologicals, Littleton, CO, USA).

Techniques: Southern Blot, Injection, Expressing, TRAP Assay, Activity Assay, Real-time Polymerase Chain Reaction

Journal: Journal of Translational Medicine

Article Title: Development of patient-derived xenograft models from a spontaneously immortal low-grade meningioma cell line, KCI-MENG1

doi: 10.1186/s12967-015-0596-8

Figure Lengend Snippet: Human meningioma mouse xenograft model KCI-MENG1-LPSX generated with the spontaneously immortal cell line KCI-MENG1-LP. Tumors from immunocompromised SCID mice were dissected ( a ) and the derivative cell line KCI-MENG1-LPSX CL was generated. The H&E staining of the mouse tumor revealed a pattern of moderately cellular meningothelial cells similar to the original patient tumor ( b ). The KCI-MENG1-LPSX CL cells were composed of the round-shaped cells similar to the high passage parent cell line KCI-MENG1-HP ( c ). The EMA, PR, and N-cadherin IHC of the mouse tumor highly resembled the original patient-derived tumor ( d top row ). The vimentin- and Ki-67-stained cells in the mouse tumor tissue were markedly more abundant and more intensely stained than in the original tumor ( d top row ). KCI-MENG1-LPSX CL cells displayed the same patterns of immunostaining as the high passage parent cell line KCI-MENG1-HP, including the loss of PR staining ( d bottom row ). Scale bar 50 µm.

Article Snippet: Primary antibodies used targeted the following proteins: EMA (cat.#247M-94), PR (cat.#323R-14), Ki-67 (cat.#275R-14), vimentin (cat.#347R-14; all from CellMarque, Rocklin, CA, USA), and N-cadherin (cat.#NBP1-48309, Novus Biologicals, Littleton, CO, USA).

Techniques: Generated, Staining, Derivative Assay, Immunostaining