orientin has been researched along with Breast-Neoplasms* in 2 studies
2 other study(ies) available for orientin and Breast-Neoplasms
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Orientin inhibits invasion by suppressing MMP-9 and IL-8 expression via the PKCα/ ERK/AP-1/STAT3-mediated signaling pathways in TPA-treated MCF-7 breast cancer cells.
Orientin (luteolin 8-C-β-D-glucopyranoside), a glycosyl dietary flavonoid, has therapeutic effects such as anti-inflammation and antiadipogenesis. However, there is little known about the antimigratory and anti-invasive effects of orientin. Thus, we demonstrate the anti-invasive effects of orientin compared with well-known anticancer flavonoid, luteolin and luteolin 8-C-β-fucopyranoside (LU8C-FP).. We investigated whether orientin would inhibit the migration and invasion of 12-O-tetradecanoyl phorbol-13-acetate (TPA) induced MCF-7 breast cancer cells.. We investigated the anti-invasive mechanism of orientin by using wound-healing assay, Matrigel invasion assay, gelatin zymography, qRT-PCR, ELISA, western blotting, nuclear, membrane and cytosolic fractionations, and immunofluorescence staining in MCF-7 cell line.. We demonstrated the antimigratory and anti-invasive effects of orientin in TPA-treated MCF-7 cells. TPA-induced membrane translocation of protein kinase C alpha (PKCα), phosphorylation of extracellular signal regulated kinase (ERK), and nuclear translocations of activator protein-1 (AP-1) and signal transducer and activator of transcription 3 (STAT3) were downregulated by orientin. In addition, orientin also inhibited matrix metalloproteinase-9 (MMP-9) and interleukin-8 (IL-8) expression.. Orientin inhibits migratory and invasive responses by suppressing MMP-9 and IL-8 expression through mitigation of TPA-induced PKCα and ERK activation, as well as the nuclear translocation of AP-1 and STAT3. Therefore, orientin prevents tumor invasion and could be applied as a possible therapeutic agent for the treatment of cancer metastasis. Topics: Breast Neoplasms; Cell Line, Tumor; Extracellular Signal-Regulated MAP Kinases; Female; Flavonoids; Glucosides; Humans; Interleukin-8; Luteolin; Matrix Metalloproteinase 9; MCF-7 Cells; Mitogen-Activated Protein Kinase 6; Neoplasm Invasiveness; NF-kappa B; Protein Kinase C-alpha; Signal Transduction; STAT3 Transcription Factor; Tetradecanoylphorbol Acetate; Tissue Array Analysis; Transcription Factor AP-1 | 2018 |
Cajanus cajan- a source of PPARγ activators leading to anti-inflammatory and cytotoxic effects.
Cajanus cajan is an important legume crop in the human diet in many parts of the world. Due to its pharmacological properties, C. cajan is, moreover, used in traditional medicine for treating skin diseases, diabetes, inflammatory disorders and various other dysfunctions. In this study, we focused on the role of peroxisome proliferator-activated receptor gamma (PPARγ) as a potential therapeutic target of Cajanus cajan and its main compounds for the treatment of cancer, inflammation and inflammation-related disorders. The anti-inflammatory potential of C. cajan and its bioactive compounds and their cytotoxicity on the human cervical adenocarcinoma cell line HeLa, the human colorectal adenocarcinoma cell line CaCo-2 and the human breast adenocarcinoma cell line MCF-7 were elucidated. C. cajan and its compounds exerted significant anti-inflammatory activity on lipopolysaccharide-stimulated macrophages, showed good cytotoxic effects on the 3 different cancer cell lines and proved PPARγ activity in vitro. The main active compounds were orientin, pinostrobin and vitexin. Cajaninstilbene acid and pinosylvin monomethylether were identified as novel PPARγ activators. Based on these data, C. cajan provides excellent beneficial medicinal attributes and may be used as a potential food or a pharmaceutical supplement. Topics: Anti-Inflammatory Agents; Antineoplastic Agents, Phytogenic; Apigenin; Breast Neoplasms; Caco-2 Cells; Cajanus; Colorectal Neoplasms; Diet; Female; Flavanones; Flavonoids; Glucosides; HeLa Cells; Humans; MCF-7 Cells; Phytotherapy; Plant Extracts; PPAR gamma; Uterine Cervical Neoplasms | 2016 |