cmt93 wt cell lines (ATCC)
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Cmt93 Wt Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 95/100, based on 260 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/cmt93+wt+cell+lines/pmc07412704-47-3-7?v=ATCC
Average 95 stars, based on 260 article reviews
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1) Product Images from "Mindin serves as a tumour suppressor gene during colon cancer progression through MAPK/ERK signalling pathway in mice"
Article Title: Mindin serves as a tumour suppressor gene during colon cancer progression through MAPK/ERK signalling pathway in mice
Journal: Journal of Cellular and Molecular Medicine
doi: 10.1111/jcmm.15332
Figure Legend Snippet: Mindin suppresses colon cancer cell proliferation in vitro. A, Analysis of CT26 WT (left side) and CMT93 (right side) cell proliferation in the mindin‐overexpressing cells and control cells by CCK‐8 assay (* P < 0.05). B, Analysis of cell proliferation in the mindin knock‐down cells and control cells by CCK‐8 assay (* P < 0.05). C, Analysis of cell proliferation in the mindin‐overexpressing cells and control cells by BrdU assay (* P < 0.05). D, Analysis of cell proliferation in the mindin knock‐down cells and control cells by BrdU assay (* P < 0.05)
Techniques Used: In Vitro, Control, CCK-8 Assay, Knockdown, BrdU Staining
Figure Legend Snippet: Subcutaneous implantation tumour growth of mindin‐overexpressing CMT93 and CT26 WT cells. C57BL/6 and BALB/c mice were subcutaneously injected with stable mindin‐overexpressing CMT93 or CT26 WT cells, or PCMV4 control cells. Tumour size was measured every 3 d for 24 d. A, Images of isolated tumours from the four groups of study mice (n = 5). B, In vivo tumour growth resulting from the mindin‐overexpressing CMT93 or CT26 WT cell (n = 5, * P < 0.05). C, Western blot analysis confirming mindin protein overexpression in the tumour tissues of the four study groups at the end of the study period. Tubulin was used as a protein loading control (n = 5). Upper panel indicates CMT93, and lower panel indicates CT26 WT among A‐C
Techniques Used: Injection, Control, Isolation, In Vivo, Western Blot, Over Expression
Figure Legend Snippet: Subcutaneous implantation tumour growth of mindin knock‐down CMT93 and CT26 WT cells. C57BL/6 and BALB/c mice were subcutaneously injected with stable mindin knock‐down CMT93 or CT26 WT cells, or PU6 control cells. Tumour size was measured every 3 d for 24 d. A, Images of isolated tumours from the four groups of study mice (n = 5). B, In vivo tumour growth resulting from the mindin knock‐down CMT93 or CT26 WT cell (n = 5, * P < 0.05). C, Western blot analysis confirming mindin protein deficiency in the tumour tissues of the four study groups at the end of the study period. Tubulin was used as a protein loading control (n = 5). Upper panel indicates CMT93, and lower panel indicates CT26 WT among A‐C
Techniques Used: Knockdown, Injection, Control, Isolation, In Vivo, Western Blot
Figure Legend Snippet: A, Sequencing chromatograms show the nucleotide mutation of mindin−/− mice using a CRISPR‐Cas system. B, Western blot analysis using antibody against mindin on mice colon tissues. Actin was used as a loading control. C, The tumour images of 21 d after subcutaneous injection of CMT93 colorectal cancer cells in mindin‐knockout and the control mice. Tumour size was measured and quantitatively analysed (n = 5, * P < 0.05). D, Mindin expression was measured by ELISA in the first day and the end point of the model in WT mice serum with or without CRC procedure. E, The cells were isolated from tumour tissues of the AOM/DSS‐induced CRC mice. The procedure of flow cytometry analysis as follows: gated the single cells first, separated cells with the LIVE/DEAD dye and gated the CD45 + cells, then right panels showed the FITC‐CD11b and PE‐F4/80‐stained cells
Techniques Used: Sequencing, Mutagenesis, CRISPR, Western Blot, Control, Injection, Knock-Out, Expressing, Enzyme-linked Immunosorbent Assay, Isolation, Flow Cytometry, Staining