Four new cardenolide monoglycosides, cardenolides N-1 (1), N-2 (2), N-3 (3), and N-4 (4), were isolated from Nerium oleander, together with two known cardenolides, 5 and 12, and seven cardenolide monoglycosides, 6-11 and 13. The structures of compounds 1-4 were established on the basis of their spectroscopic data. The in vitro anti-inflammatory activity of compounds 1-13 was examined on the basis of inhibitory activity against the induction of the intercellular adhesion molecule-1 (ICAM-1). Compounds 1, 5, 6, and 11-13 were active at an IC50 value of less than 1 microM. The cytotoxicity of compounds 1-13 was evaluated against three human cell lines, normal human fibroblast cells (WI-38), malignant tumor cells induced from WI-38 (VA-13), and human liver tumor cells (HepG2). Compounds 1, 4, 6, and 11-13 were active toward V-13 cells, and compounds 1, 11, and 12 were active toward HepG2 cells at IC50 values of less than 1 microM. Compounds 4, 5, 10, and 12 showed selective cell growth inhibitory activity toward V-13 tumor cells compared with that of parental normal WI-38 cells. The MDR-reversal activity of compounds 1-13 was evaluated on the basis of the amount of calcein accumulated in MDR human ovarian cancer 2780AD cells in the presence of each compound. Compounds 4, 9, and 10 showed significant effects on calcein accumulation, compound 4 showing stronger activity than that of verapamil.

Long non-coding RNAs (lncRNAs) are considered to be important regulators in breast cancer. In the present study, the potential mechanisms and functional roles of lncRNA PSMG3-antisense (AS)1 were investigated in vivo and in vitro. The relative expression levels of lncRNA PSMG3-AS1 and microRNA (miR)-143-3p were determined using reverse-transcription quantitative PCR. The protein expression levels of collagen type 1 alpha 1 (COL1A1) and proliferating cell nuclear antigen (PCNA) were obtained using western blot analysis. Bioinformatics analysis was used to identify the relationship between PSMG3-AS1, miR-143-3p and COL1A1. Colony forming and Cell Counting Kit-8 assays were used to detect cell proliferation. Transwell and wound-healing assays were used to determine cell migration. The results of the present study demonstrated that PSMG3-AS1 expression was increased in breast cancer tumor tissues and cell lines, and that of miR-143-3p was decreased. Knockdown of PSMG3-AS1 increased the level of miR-143-3p expression, which led to the mitigation of proliferation and migration capacity in breast carcinoma cells. Additionally, PSMG3-AS1 knockdown was demonstrated to reduce the mRNA and protein expression levels of COL1A1. miR-143-3p mimic transfection reduced proliferation and migration in MDA-MB-231 and MCF-7 cell lines. Furthermore, miR-143-3p inhibition significantly increased the proliferation and migration of breast cancer cells compared with the negative control group. The mRNA and protein expression levels of PCNA were reduced in the MCF-7 cell line when transfected with miR-143-3p mimics and si-PSMG3-AS1. However, PCNA expression was increased in cells transfected with a miR-143-3p inhibitor. In conclusion, the results of the present study identified a novel lncRNA PSMG3-AS1, which serves as a sponge for miR-143-3p in the pathogenesis of breast cancer. PSMG3-AS1 may be used as a potential therapeutic target gene in breast cancer treatment.

Five new triterpene saponins named phytolaccasaponins N-1 (1), N-2 (2), N-3 (3) N-4 (4), and N-5 (5) were isolated from the roots of Phytolacca americana together with seven known triterpene saponins (6-12). The structures of the five new saponins were established as shown in structures 1-5 on the basis of their spectroscopic data. The MDR-reversal activity of 1-12 was evaluated on the basis of the amount of calcein accumulated in MDR human ovarian cancer 2780 AD cells in the presence of each compound. The most effective compound was 8 (155% of control at 25 microg/mL).