tramp c2ras prostate tumor cells  (ATCC)

Journal: Biomolecules

Article Title: Induced Tumor-Suppressing (iTS) Cell-Based Approach for Protecting the Bone from Advanced Prostate Cancer

doi: 10.3390/biom16020240

Figure Lengend Snippet: Inhibitory effects of CM Oy-Lrp5 on TRAMP-C2ras prostate tumor cells. CN = control, CM = conditioned medium, Oy CM = osteocyte-derived CM, and Lrp5 = Lrp5 overexpression. The data are presented as mean ± S.D. (n = 3). The double asterisks indicate p < 0.01. ( a ) Inhibition of MTT-based viability of TRAMP-C2ras prostate tumor cells by CM Oy-Lrp5 . ( b ) Reduction in EdU-based proliferation by CM Oy-Lrp5 . Scale bar: 200 µm. ( c ) Increase in FRET efficiency in the vinculin biosensor by CM Oy-Lrp5 . The observed increase in FRET efficiency implies a decrease in vinculin-mediated molecular force at focal adhesions. Scale bar: 20 µm. ( d ) Inhibition of scratch-based migration of TRAMP-C2ras prostate tumor cells by CM Oy-Lrp5 . Scale bar: 200 µm. ( e ) Inhibition of transwell invasion by CM Oy-Lrp5 . Scale bar: 200 µm. ( f ) Reduction in the growth of 3D tumor spheroids by CM Oy-Lrp5 . Scale bar: 200 µm.

Article Snippet: TRAMP-C2ras prostate tumor cells (ATCC, CRL-2731) were cultured in DMEM/F-12 medium as described [ ].

Techniques: Control, Derivative Assay, Over Expression, Inhibition, Migration

Journal: Cell Reports Medicine

Article Title: Optimized arenaviruses with tumor-tropic mutations promote safe anti-tumor efficacy via sustainable immune modulatory properties

doi: 10.1016/j.xcrm.2025.102411

Figure Lengend Snippet: Analysis of different combinations of fast evolution mutations (A) Infection assays (MOI = 0.1, 16 h) of different human cancer cells (lung adenocarcinoma: H1975 and A549; primary sarcoma: Gist-T1; melanoma metastasis: MaMel86a and MaMel51), myotubes and human skeletal muscle myoblasts (HSMM) ( n = 4–6; duplicates in 2–3 experimental replicates) with different recombinant viruses carrying a point mutation in the respective position. Notably, the GP mutation 492I always occurred alongside one single NP mutation. Hence, in all further analyses, the mention of mutation 492I mutation inherently includes the NP mutation, even if not explicitly stated. (B) Infection assays (MOI = 0.1, 16 h) of different murine cancer cells (oropharyngeal carcinoma: MOPC; Lewis lung carcinoma: LLC; prostate adenocarcinoma: TrampC2; colon adenocarcinoma: MC38) and human cancer cells (lung adenocarcinoma: H1975 and A549; melanoma metastasis: MaMel86a and MaMel51) ( n = 6; duplicates in 3 experimental replicates) using different recombinant viruses carrying specific point mutations. (C) Spider plots showing the factor of acceleration in propagation of the mutations tested in various human and murine tumor cells. The mean ratio for each mutated virus is given ( n = 4–6; duplicates in 2–3 experimental set ups). (D) Entry assay on human lung adenocarcinoma (A549) cells and A549-αDG knockout cells of recombination virus GP181M-185W-492I and control virus ( n = 6; duplicates in 3 independent experiments). (E) A549 lung adenocarcinoma cells were treated with CD164 blocking antibody or isotype control for 1 h and subsequently infected with the recombination virus GP181M-185W-492I (MOI 10) for 1, 5, and 15 min. The number of viral particles outside the cells per one cell is shown ( n = 6 cells analyzed per sample, ∗∗ p < 0.01). (F and G) Representative pictures for cells treated with isotype control (scale bars: left = 2 μm, right = 200 nm) (F) and CD164 blocking antibody (scale bars: left = 2 μm, right = 200 nm) (G) for 1 min of infection are shown. (H) Infection assays (MOI = 0.1, 16 h) of different human cancer cells (thyroid anaplastic carcinoma: Cal62, C643, 8305C, and 8505C; epidermoid carcinoma: A431; lung adenocarcinoma: KRAS-mutated: A549 and H23; EGFR-mutated: H1975, Alk-rearranged: H2228, WT/other: H1299, H1355, H1792, and H1373; small cell lung cancer: HCC-44; endocervical adenocarcinoma: HeLa; fibroblast liposarcoma: SW-872; colon adenocarcinoma: SW-480; bronchiole lung carcinoma: H358; hepatocellular carcinoma: HepG2) ( n = 6–8; duplicates in 3–4 experimental set ups) comparing WE, recombinant WE-CL13 and a recombinant virus carrying three point mutations as shown. For statistical analysis, WE-CL13-GP181M-185W-492I was compared to both WE and WE-CL13. (I) Hepatocytes ( n = 3; biological replicates; separate flasks), melanocytes ( n = 3; biological replicates; separate flasks), epithelial cells (InEpc, n = 3; biological replicates; separate flasks) and alveolar cells (ALI-cultures, n = 6; duplicates of 3 different patients) were infected with WE or WE-CL13-GP181M-185W-492I. Number of infected cells was determined 24 h with flow cytometry. For statistical analysis, the WE-CL13-GP181M-185W-492I virus was compared to the mock-infected control, but no significant difference was observed. However, a statistical difference between WE and WE-CL13-GP181M-185W-492I was detected. Data are presented as the mean ± SEM; ns = not significant, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001 by t test (D, E, H, and I).

Article Snippet: TrampC2 , ATCC , CRL-2731.

Techniques: Infection, Recombinant, Mutagenesis, Virus, Knock-Out, Control, Blocking Assay, Flow Cytometry