Objective Wnt signaling plays an important role in the development and progression of renal cell carcinoma (RCC).This study aimed to evaluate the effects of the Wnt signaling inhibitor 15-oxospiramilactone on the proliferation , migration, cell apoptosis, and cycles of the human RCC cell line 786-0, and to investigate the possible mechanisms of this small molecule acting on RCC in ivtro. Methods We treated 786-0 cells with DMSO ( blank control group ) and 15-oxospiramilactone at the concentrations of1.25μmol/L (low 15 -OSL), 2.5μmol/L (medium 15-OSL), and 5μmol/L (high 15-OSL), respectively, for 72 hours.Then we observed the changes in the proliferation and migration of the 786-0 cells by MTT and scratch-wound assay and determined their apopto-sis and cycles by Annexin V-FITC/PI assay and flow cytometry . Results 15-oxospiramilactone significantly inhibited the growth of the 7860-cells, with the IC 50of 1.088 μmol/L at 72 hours, and decreased their migration distance (P<0.05).After 36 hours of treatment, the apoptosis rates of the 786-0 cells in the low, medium, and high 15-OSL groups were (12.17 ±0.56), (18.54 ± 1.07), and (50.74 ±1.28) %, respectively, significantly increased as compared with (7.85 ±0.42) %in the blank control group (P<0.05), and in an obviously concentration-dependent manner.15-oxospiramilactone remarkably reduced the number of cells in the G0/G1 phase and increased that in the G 2/M phase (P<0.05). Conclusion 15-oxospiramilactone can significantly inhibit the pro -liferation and migration and induce the apoptosis of 786-0cells in vitro.It may be a potential anti-RCC agent.

Breast cancer is the most diagnosed cancer in women worldwide and the leading cause of most cancer-related deaths, posing a serious threat to women′s health worldwide. At present, although the prognosis of some patients with breast cancer has improved, the emergence of drug resistance and the metastasis and recurrence of breast cancer are still the main reasons for poor prognosis. CD36 is a multiligand transmembrane glycoprotein expressed on various cell types. In recent years, studies have confirmed that CD36 can reshape the lipid metabolism of cancer cells; promote the differentiation of tumor-related macrophages into M2 type and recruitment into tumor tissues; regulate the function of Treg cells, CD8+ T cells, DCs, and other immune cells, and thus promote tumor development. In addition, CD36 is also associated with breast cancer stem cells, metastasis-initiating cells, and breast drug resistant cells. Therefore, CD36 could be an important potential therapeutic target for breast cancer.