Fig. 8

SCAT7 is a potential therapeutic target for different tumor types. a Tumor growth in Balb/c nude mice 8 weeks after subcutaneous inoculation of 1 × 10⁶ Csh or SCAT7-sh2 786-O cells (n = 8 each group). b Tumors from Balb/c nude mice after subcutaneous injection of 1 × 10⁶ Csh or SCAT7-sh1 or SCAT7-sh2 A549 cells for 8 weeks (n = 6 for each group). In a and b tumor volumes (cm³) are expressed as mean ± SD, compared with Csh. c Tumor growth inhibition (TGI) for A549 subcutaneous Balb/c nude xenografts treated with 60 pmol of SCAT7 antisense oligonucleotides, LNA-1 and LNA-2, respectively, for a total of four injections (n = 5 for each group). d Average tumor growth of the xenografts treated with control or SCAT7 LNAs was calculated at each injection as follows: Vtx-Vt0. e Real-time qPCR of SCAT7 in A549 tumors collected after treatment with Ctrl-LNA, SCAT7-LNA1, and SCAT7-LNA2. The red bar represents a tumor treated with LNA2, but no downregulation was observed. Values are normalized to endogenous GAPDH. f Scatter plot showing the correlation between SCAT7 expression in vivo and the tumor volumes. The red dot represents the tumor that had no significant downregulation of SCAT7 upon LNA treatment. g Immunohistochemistry images of Ki67 staining and TUNEL assay for A549 xenografts treated with Ctrl-LNA, SCAT7-LNA-1, and SCAT7-LNA-2 (blue: DAPI, green: TUNEL-GFP). h Patient-derived xenograft (PDX) of NSG mice models treated with 100 pmol of Ctrl-LNA or SCAT7-LNA1 for a total of five injections (n = 6 for each group). i Average growth of tumor volumes of the PDX models treated with control or SCAT7 LNAs. j, k Model depicting the functional involvement of SCAT7 in regulating cancer hallmarks (j) and mechanism of FGF/FGFR signaling regulation by SCAT7 (k). The statistical significance shown in b–e and i was derived using a two-tailed unpaired Student’s t-test. Data are plotted as mean ± SD (*p ≤ 0.05; **p = 0.01 ̶ 0.001; ***p < 0.001)