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

Journal: International Journal of Molecular Sciences

Article Title: Depletion of Lipocalin 2 (LCN2) in Mice Leads to Dysbiosis and Persistent Colonization with Segmented Filamentous Bacteria

doi: 10.3390/ijms222313156

Figure Lengend Snippet: Comparative analysis of the intestine macroscopical parameters and expression of Lcn2 in wild type (n = 4) and Lcn2 -/- mice (n = 4 or 5). ( A ) Evaluation of the body weight of male animals at the same age (left). Corresponding ceca were prepared and weighed (middle). Ratio of body to cecal weight (right). ( B ) Gross macroscopical and graphical comparison of the total small and large intestinal lengths measured (n = 4 or 5). ( C ) Quantitative analysis of Lcn2 mRNA (upper) and LCN2 protein expression (lower) in the distal small intestine (left) cecum (middle), and distal colon (right) of wild type ( Lcn2 +/+ ) and Lcn2 null mice (each n = 4 or 5). Relative mRNA expression of respective genes was done by RT-qPCR and normalized to Gapdh or β-actin . Equal protein loading was demonstrated by re-probing the membranes with a specific antibody directed against GAPDH or β-actin. E-cadherin was probed as a marker for epithelial-to-mesenchymal transition (EMT). Primers used are given in . Statistical evaluation in ( A – C ) was performed by an unpaired t -test, whereby the difference of two samples from a level of p < 0.05 is considered statistically significant (*: p < 0.05, **: p < 0.01, ***: p < 0.001).

Article Snippet: For detection of individual proteins, the primary antibodies for LCN2/NGAL (AF3508, R & D Systems, Abingdon, UK), GAPDH (6C5) (sc-32233, Santa Cruz, Biotech, Santa Cruz, CA, USA), β-actin (A5441, Sigma–Aldrich, MI, USA), and E-cadherin (AP20195PU-N, OriGene, Rockville, MD, USA) were diluted in 2.5% ( w / v ) non-fat milk powder in TBST.

Techniques: Expressing, Comparison, Quantitative RT-PCR, Marker

Journal: Oncotarget

Article Title: Mutant p53 induces EZH2 expression and promotes epithelial–mesenchymal transition by disrupting p68-Drosha complex assembly and attenuating miR-26a processing

doi:

Figure Lengend Snippet: A. Tumor growth curve in nude mice. After tumor cells were injected subcutaneously into the neck of nude mice, the short and long diameters of the tumors were measured every 5 days and tumor volumes (mm3) were calculated. B. The nude mice with tumor formations. C. Photograph of tumors derived from LV-miR-26a, LV-miR-26a Ctrl or untransfected HEC-1B cells in nude mice. D. Weights of tumors. * P < 0.05 as compared with either untreated group or LV-miR-26a Ctrl group. E. Representative HE staining histopathologic image of tumor tissues in mice (left panel). Vimentin, E-cadherin, EZH2, and Ki67 expression of tumors were detected by immunohistochemical technique (right panel). F. ~ I. Quantification of Vimentin, E-cadherin, EZH2, and Ki67 expression in E. * P < 0.01.

Article Snippet: Total cell lysis and western blot analysis were performed as described previously using the following antibodies [ ]: EZH2 (5246; 1:1000; CST), p53 (2527; 1:1000; CST), N-cadherin (13116; 1:1000; CST), E-cadherin (3195; 1:1000; CST), Vimentin (5741; 1:1000; CST), Snail (3879; 1:1000; CST) and GAPDH (5632-1; 1:2000; Epitomics), and anti-rabbit IgG (1:10000, Jackson).

Techniques: Injection, Derivative Assay, Staining, Expressing, Immunohistochemical staining