Journal: Frontiers in Oncology

Article Title: Schwann Cell-Derived CCL2 Promotes the Perineural Invasion of Cervical Cancer

doi: 10.3389/fonc.2020.00019

Figure Lengend Snippet: The crosstalk between SCs and cervical cancer cells. (A) DM promotes cell migration of HeLa and ME-180 cells compared with CM. DM, DRG medium; CM, Control medium. ( B) Cocultivation of DRGs with HeLa cells. Images from confocal microscopy shows the process of a cancer cell (marked by asterisks) toward the center of the DRG. Assume that the time of the first picture is 0 h. The SCs are marked by white arrows. The smaller white dotted lines describe the border of the DRG and the larger defines the Matrigel edge. (C) HeLa and ME-180 cells upregulated the expression of MMP2/9/12 in SCs. * P < 0.05, ** P < 0.01, *** P <0.001.

Article Snippet: After blocking in 5% non-fat milk in 1 × TBST for 1 h, the membranes were incubated at 4°C overnight with primary antibodies including CCR2 (12199S, Cell Signaling Technology), MCP1 (ab25124, Abcam), MMP9 (ab76003, Abcam), MMP2 (ab92536, Abcam), MMP12 (ab52897, Abcam) and β-actin (CST-5174T, Cell Signaling Technology), and EMT Antibody Sampler Kit (CST-9782, Cell Signaling Technology).

Techniques: Migration, Control, Confocal Microscopy, Expressing

Journal: PLoS ONE

Article Title: Loss of p120ctn causes EGFR-targeted therapy resistance and failure

doi: 10.1371/journal.pone.0241299

Figure Lengend Snippet: (A) Cell viability assays in EPC1-C, -P, -E, and -PE cells show that EPC1-PE cells are resistant to EGFR therapy-induced death, (n = 8). (B) Cell viability assays show that EPC2-PE cells are resistant to cell death, (n = 4). Vehicle control was DMSO. * denotes p<0.05 for gefitinib treatment comparisons between EPC-E vs. EPC-C and EPC-PE vs. EPC-E. # denotes p<0.05 for erlotinib treatment comparisons between EPC-E vs. EPC-C and EPC-PE vs. EPC-E. ^ denotes p<0.05 for cetuximab treatment comparisons between EPC-E vs. EPC-C and EPC-PE vs. EPC-E.

Article Snippet: For viability testing, cells were treated with 5 μM gefitinib (#076091; Matrix Scientific, Columbia, SC), 10 μM erlotinib (#10483; Cayman Chemical; Ann Arbor, MI), or 10 nM cetuximab (#NBP2-75903; Novus Biologicals; Centennial, CO), with or without BAY 11–7085 (#B3033; ApexBio Technology; Houston, TX) at 2 μM or 3.3 μM for 48 hours.

Techniques: Control

Journal: PLoS ONE

Article Title: Loss of p120ctn causes EGFR-targeted therapy resistance and failure

doi: 10.1371/journal.pone.0241299

Figure Lengend Snippet: (A) A dose response curve for BAY 11–7085 using EPC1 cells demonstrates no significant cell death in any cell line at 2 uM. (B) Western blot analysis demonstrates a decrease in pNFkB expression when cells are treated with 2 uM BAY 11–7085. (C) Cell viability assays demonstrate that treatment of EPC1 cells with 2 uM BAY 11–7085 in combination with either gefitinib, erlotinib, or cetuximab results in a partial reduction in cell viability in EPC1-PE cells (n = 3). Vehicle refers to cells treated with 2 uM BAY 11–7085 and DMSO (as the EGFR diluent). * denotes p<0.05 for gefitinib treatment comparisons between EPC-E vs. EPC-C and EPC-PE vs. EPC-E. # denotes p<0.05 for erlotinib treatment comparisons between EPC-E vs. EPC-C and EPC-PE vs. EPC-E. ^ denotes p<0.05 for cetuximab treatment comparisons between EPC-E vs. EPC-C and EPC-PE vs. EPC-E.

Article Snippet: For viability testing, cells were treated with 5 μM gefitinib (#076091; Matrix Scientific, Columbia, SC), 10 μM erlotinib (#10483; Cayman Chemical; Ann Arbor, MI), or 10 nM cetuximab (#NBP2-75903; Novus Biologicals; Centennial, CO), with or without BAY 11–7085 (#B3033; ApexBio Technology; Houston, TX) at 2 μM or 3.3 μM for 48 hours.

Techniques: Western Blot, Expressing