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