An Antioxidant Polysaccharide from Ganoderma lucidum Induces Apoptotic Activity in Breast Cancer Cell Line

The purpose of this study is to elucidate the apoptotic activity of Ganoderma lucidum polysaccharide (GLP) in a human breast cancer cell line MCF-7 in vitro. According to DPPH assay, GLP showed a good antioxidant (IC 50 value is 202.4 µg/mL). Based on MTT assay, the results showed that GLP inhibits MCF-7 cells proliferation in a dose- and time- dependent manner (p<0.001). IC 50 values of the cytotoxicity of GLP and doxorubin were 110.907 µg/mL and 58.206 µg/mL respectively. The results from the flow cytometry indicated that GLP could induce apoptotic activity through inducing the up-regulation of the Bax and Caspase-9 and the down-regulation of the BcL-2 in MCF-7 cells. At 2×IC 50 , GLP increased the early-apoptotic and dead cells of MCF-7 from 18.23% to 34.76% and 8.45% to16.34% respectively. In conclusion, the GLP shows anticancer activity against MCF-7 through preventing the proliferation and inducing the apoptosis of MCF-7 cells. Our data provide the potential molecular targets in cancer prevention and reveal the key barriers in the current anticancer drugs development.

Investigation of Chemopreventive and Antiproliferative Potential of Dicliptera roxburghiana

Context: Carcinogenesis causes much human misery. It is a process involving multistage alterations. Medicinal plants are candidates for beneficial anticancer agents. Objectives: Investigation of anticancer proficiencies of the plant Dicliptera roxburghiana. Material and methods: Crude extract and derived fractions were inspected for their inhibitory potential against nuclear factor KB (NFκB), nitric oxide synthase inhibition, aromatase inhibition and induction of quinone reductase 1 (QR 1). Antiproliferative activity was determined by using various cancer cell lines for example hormone responsive breast cancer cell line MCF-7, estrogen receptor negative breast cancer cell line MDA-MB-231, murine hepatoma cells Hepa 1c1c7, human neuroblastoma cells SK-N-SH and neuroblastoma cells MYCN-2. Results: Ethyl acetate and n-butanol fractions of D. roxburghiana were strongly active against NFκB with IC50 of 16.6 ± 1.3 and 8.4 ± 0.7 µg/ml respectively with 100% survival. Chloroform fraction of the plant exhibited an induction ratio of 2.4 ± 0.09 with CD value of 17.7 µg/ml. Regarding the nitrite assay, the n-hexane fraction exhibited significant inhibition of NO activity with IC50 of 17.8 ± 1.25 µg/ml. The n-butanol fraction exhibited strong antiproliferative activity against IcIc-7 cell lines with IC50 values of 13.6 ± 1.91 µg/ml; against MYCN-2 a cytotoxic effect developed with dose dependence, with IC50 of 12.6 ± 1.24 µg/ml. In antiproliferative activity against SK-N-SH cell lines, chloroform, ethyl acetate and n-butanol fractions were efficiently active with IC50 values of 11.2 ± 0.84, 14.6 ± 1.71 and 16.3 ± 1.57 respectively. Discussion and Conclusion: It was demonstrated that various fractions of D. roxburghiana displayed appreciable anticancer characteristics and could be a potent source for the development of anticancer leads.

Effects of Metformin on Human Bone-derived Mesenchymal Stromal Cell – Breast Cancer Cell Line Interactions

Metformin is used to treat patients with type 2 diabetes mellitus and was found to lower the incidence of cancer. Bone metastasis is a common complication of advanced breast cancer. The present study investigated the effects of metformin on human bone-derived mesenchymal stromal cells (BM-MSC) – breast cancer cell line interactions. BM-MSCs grown from box chisels were tested for growth-stimulating and migration-controlling activity on four breast cancer cell lines either untreated or after pretreatment with metformin. Growth stimulation was tested in MTT tests and migration in scratch assays. Furthermore, the expression of adipokines of BM-MSCs in response to metformin was assessed using Western blot arrays. Compared to breast cancer cell lines (3.6 ± 1.4% reduction of proliferation), 500 µM metformin significantly inhibited the proliferation of BM-MSC lines (12.3 ± 2.2 reduction). Pretreatment of BM-MSCs with metformin showed variable effects of the resulting conditioned media (CM) on breast cancer cell lines depending on the specific BM-MSC –cancer line combination. Metformin significantly impaired the migration of breast cancer cell lines MDA-MB-231 and MDA-MB-436 in response to CM of drug-pretreated BM-MSCs. Assessment of metformin-induced alterations in expression of adipokines by BM-MSC CM indicated increased osteogenic signaling and possibly impairment of metastasis. In conclusion, the anticancer activities of metformin are the result of a range of direct and indirect mechanisms that lower tumor proliferation and progression. A lower metformin-induced protumor activity of BM-MSCs in the bone microenvironment seem to contribute to the positive effects of the drug in selected breast cancer patients.

Serological Changes of Monoclonal Antibody CAMA3C8 against Human Breast Cancer Cell Line

Background: Tumor associated antigen are glycoproteins and glycolipids expressed on the surface or in the cytoplasm of tumor cells. The antigenic components are shed from the tumor cells into the tissue culture medium or blood or other human body fluids like human milk. Objective: In the present study, investigate the serological assay of the antigen recognized by CAMA3C8 in patients with carcinoma of the breast. Methods: The study is desgriptive cross section study.The study was divited into four groups based on the expression of tumor associated antigen. Results: In breast cancer CAMA3C8 levels were significantly increased in stage 4 when compared with stage 1 breast cancer cell line. Conclusion: In the present study, we conclude that significantly recognized CAMA3C8 defined antigens in breast cancer.