Rakicidin J and K, two cytotoxic and antibacterial cyclic depsipeptides from the marine bacterium Micromonospora chalcea.

Rakicidin J (1) and rakicidin K (2), two new cyclic depsipeptides, were isolated from culture broth of Micromonospora chalcea FIM-R150103. Their structures were elucidated by extensive analysis of NMR, HR-ESI-MS, and electronic circular dichroism (ECD) data. The two compounds showed strong cytotoxic activity against human colon carcinoma HCT-8 and human pancreatic cancer PANC-1 cells under normoxic and hypoxic conditions in the range of IC50 values from 0.024 to 0.79 µg/mL. Moreover, compounds 1 and 2 also showed moderate antibacterial activity against ten Gram-positive bacterial strains with MIC values ranging from 4 to more than 32 µg/mL. Structure-activity relationship of these two compounds with a close analogue, rakicidin B1, is also discussed.

Structure elucidation and antitumour activity of a new macrolactam produced by marine-derived actinomycete Micromonospora sp. FIM05328.

Chemical investigation of a marine-derived actinomycete strain Micromonospora sp. FIM05328 isolated from a soil sample collected from the East China Sea, resulted in the discovery of a new 26-membered polyene macrolactam metabolite FW05328-1 (1), together with a known polyene with pyridone ring compound aurodox (2). The structures of compounds 1 and 2 were determined by the detailed analysis of 1D, 2D NMR and HR-TOF-MS data, along with literature data analysis. 1 and 2 exhibited excellent antiproliferative activities against KYSE30, KYSE180 and EC109 human tumour cell lines, but displayed no antibacterial activities against bacteria or fungi were tested.

Screening of potential probiotic lactic acid bacteria based on gastrointestinal properties and perfluorooctanoate toxicity.

The consumption of lactic acid bacteria capable of binding or degrading food-borne carcinogens may reduce human exposure to these deleterious compounds. In this study, 25 Lactobacillus strains isolated from human, plant, or dairy environments were investigated for their potential probiotic capacity against perfluorooctanoate (PFOA) toxicity. The PFOA binding, tolerance ability, and acid and bile salt tolerance were investigated and assessed by principal component analysis. Additionally, the effect of different pH levels and binding times was assessed. These strains exhibited different degrees of PFOA binding; the strain with the highest PFOA binding capability was Lactobacillus plantarum CCFM738, which bound to 49.40 ± 1.5 % of available PFOA. This strain also exhibited relatively good cellular antioxidative properties, acid and bile salt tolerance, and adhesion to Caco-2 cells. This study suggests that L. plantarum CCFM738 could be used as a potential probiotic in food applications against PFOA toxicity.

FW523-3, a novel lipopeptide compound, induces apoptosis in cancer cells.

FW523-3, a new lipopeptide compound, was recently isolated and purified from the culture broth of a marine Micromonospora chalcea. FW523-3 was shown to inhibit the proliferation of certain cancer cells. However, the spectra and the underlying mechanism of its antitumor activity are unclear. In this study, the MTT and colony formation assays were employed to determine the antitumor spectra of FW523-3 and its effect on cell proliferation, respectively. Apoptosis was analyzed using DNA laddering assay and flow cytometry and the involved pathways were explored by Western blotting. Results revealed that FW523-3 exhibited cytotoxicity in a panel of tumor cell lines including esophageal squamous cell carcinoma cells (EC109), lung cancer cells (A549 and 95D), gastric cancer cells (SGC7901), uterine cervix cancer cells (HeLa) and hepatocellular carcinoma cells (HepG2). Based on these results, FW523-3 inhibited the colony formation ability of tumor cells. Moreover, FW523-3 induced apoptosis via activation of caspases 9, 7 and 3. FW523-3 also blocked the ERK and p38 signaling pathways. Taken together, we propose that FW523-3 acts as a broad-spectrum antitumor drug. FW523-3 inhibits tumor cell growth and induces tumor cell apoptosis via the mitochondrial and MAPK pathways.