In vivo and in vitro experiments validated the effect of SIGLEC15 on breast cancer proliferation and explored therapeutic strategies based on its expression level. (IMAGE)
Caption
(A) Comparison of the cell proliferation between overexpression and control group of the BT549 and MB231 cells using the CCK8 method. (B) Quantitative analysis of the colony formation assay in BT549 and MB231. (C) SHES and SLES in TCGA-BRCA were analyzed for differences in the drug resistance of Nutlin-3a through IC50 analysis. (D, E) CCK-8 assay and colony formation assay were used to evaluate the therapeutic effect of Nutlin-3a on SIGLEC15-overexpressing BT549 and MB231 cells. (F, G) CCK-8 and colony formation assays verified the inhibitory effect of carboplatin on SIGLEC15-knockdown MB231 cells. (H) MB231 cells (vector and SIGLEC15 groups) were subcutaneously injected into the left mammary fat pads of 4-week-old female BALB/c nude mice. Beginning on day 10 post-injection, the mice received daily intraperitoneal injections of either Nutlin-3a (5 mg/kg) or physiological saline (control). Tumor size was measured after the mice were euthanized. Representative tumor images were captured for each group (n = 5 mice/group). Statistical analysis of the final tumor size and mouse body weight was performed. (I) MB231 cells (shCrtl and shSIGLEC15 groups) were subcutaneously injected into the left mammary fat pads of 4-week-old female BALB/c nude mice. Beginning on day 10 post-injection, the mice received intraperitoneal injections of either carboplatin (60 mg/kg) or physiological saline (control) each week. Tumor size was measured every 3 days for 30 days after the mice were euthanized. Representative tumor images were captured for each group (n = 5 mice/group). Statistical analysis of the final tumor size and mouse body weight was performed. “ns” represents not significant, * P ≤ 0.05. ** P ≤ 0.01. *** P ≤ 0.001.
Credit
ZhaoFu Tan, Hongbin Xin, Jian Chen, Ming Lei, Gang Tu, Lingfeng Tang
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