Gastric cancer (GC) is one of the most common malignancies worldwide; however, treatment options other than surgery remain limited. Neoadjuvant chemotherapy has the potential to suppress of gastric tumorigenesis. Garcinol has been reported to exert inhibitory effects on the progression of numerous carcinomas. However, its effects in GC remain unclear. Therefore, the aim of the present study was to investigate the effects of garcinol on the proliferation, invasion and apoptosis of gastric carcinoma cells and then to explore the underlying mechanisms. Garcinol significantly decreased the proliferation and invasion of GC cells and increased apoptosis in a dose-dependent manner. Additionally, the expression of AKTp-Thr308, cyclin D1, Bcl-2, BAX, matrix metalloprotease (MMP-2) and MMP-9 in HGC-27 cells following treatment with garcinol. The results obtained in the present study suggested that garcinol may inhibit gastric tumorigenesis by suppressing the PI3K/AKT signaling pathway.

Most patients with advanced leukemia eventually die from multidrug resistance (MDR). Chemotherapy-resistant leukemia cells may lead to treatment failure and disease relapse. Overexpression of ATP-binding cassette subfamily G member 2 (ABCG2) leads to MDR, which serves as a potential biomarker and target of therapeutic intervention for leukemia cells. Targeting ABCG2 is a potential strategy for selective therapy and eradicate MDR cells, thus improving malignant leukemia treatment. KD025 (SLx-2119) is a novel Rho-associated protein kinase 2-selective inhibitor, which has been shown to inhibit adipogenesis in human adipose-derived stem cells and restore impaired immune homeostasis in autoimmunity therapy. The present study demonstrated that KD025 improved the efficacy of antineoplastic drugs in ABCG2-overexpressing leukemia cells and primary leukemia blast cells derived from patients with leukemia. Moreover, KD025 significantly inhibited the efflux of [3H]-mitoxantrone and hence accumulated higher levels of [3H]-mitoxantrone in HL60/ABCG2 cells. However, mechanistic research indicated that KD025 did not alter the protein levels and subcellular locations of ABCG2. KD025 may restrain the efflux activity of ABCG2 by obstructing ATPase activity. Taken together, KD025 can sensitize conventional antineoplastic drugs in ABCG2-overexpressing leukemia cells by blocking the pump function of ABCG2 protein. The present findings may provide a novel and useful combinational therapeutic strategy of KD025 and antineoplastic drugs for leukemia patients with ABCG2-mediated MDR.

Studies have revealed that β-asarone exerts a powerful inhibitory effect on the proliferation of human cancer cells. The authors' previous study demonstrated that β-asarone could induce LoVo colon cancer cell apoptosis in vitro and in vivo, indicating its anticancer properties. The present study aimed to determine the antineoplastic effect of β-asarone in HCT116 colon cancer cells. An in vitro proliferation assay using a real time cell analyzer demonstrated that β-asarone effectively decreased HCT116 cell proliferation in a dose-dependent manner. Bioinformatics analysis revealed that differentially expressed genes following β-asarone inhibition were involved in the 'cell cycle', 'cell division', 'cell proliferation' and 'apoptosis'. Subsequently, a xenograft assay evidenced the inhibitory effect of β-asarone on the growth of HCT116 tumors in vivo. Further detection of immune-associated cytokines and cells suggested that β-asarone might be involved in the antitumor immune response by stimulating granulocyte-colony stimulating factor and increasing the number of macrophage cells in the spleen. Additionally, a murine model of splenic-transplantation verified the strong suppressive role of β-asarone in colon cancer liver metastasis in vivo. Taken together, the results of the current study revealed that β-asarone decreased HCT116 colon cancer cell proliferation and liver metastasis potentially by activating the innate immune system, supporting the multi-system regulation theory and providing a basis for further mechanistic studies on colon cancer.