fig1

Transfer of <i>miR-100</i> and <i>miR-125b</i> increases 3D growth and invasiveness in recipient cancer cells

Figure 1. Expression levels of miR-100 and miR-125b in CC, CC-CR and ΔmiR-100/miR-125b cell lines. (A) One of multiple transcription start sites within the 330 kb MIR100HG locus encodes a 115 kb transcript that is spliced (black exons) to generate a 3 kb lncRNA (MIR100HG) with miR-100, miR-125b, let-7a, and the BLID protein encoded in the third intron. In CC-CR cells, MIR100HG, miR-100, and miR-125b are highly overexpressed, but let-7a and BLID are not[8]; (B) CC-CR cells are cetuximab-resistant cells derived from cetuximab-sensitive CC cells[8]. miR-100 and miR-125b are dramatically overexpressed in CC-CR cells, as measured by RT-qPCR. Data (mean ± SEM, n = 3) were analyzed using Student’s t test; (C) RT-qPCR analysis of miR-100 and miR-125b levels in CC-CR, ΔmiR-100, ΔmiR-125b, and ΔmiR-100/miR-125b cell lines. Fold changes were determined using the ΔΔC(t) method. Data (mean ± SEM, n = 3) were analyzed using one-way ANOVA tests with ** indicating P < 0.005, *** indicating P < 0.001, and **** indicating P < 0.0001. CC: Cystic colonies; RT-qPCR: reverse transcription-quantitative polymerase chain reaction; SEM: scanning electron microscopy; ANOVA: analysis of variance.

Extracellular Vesicles and Circulating Nucleic Acids
ISSN 2767-6641 (Online)
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