maslinic acid/neoplasms

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Maslinic acid induced apoptosis in bladder cancer cells through activating p38 MAPK signaling pathway.

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Bladder cancer is among the most aggressive human malignant carcinoma and always showed resistance to traditional chemotherapy based on DNA damaging drugs. Unlike the existing drugs that damage nuclear acid molecules, maslinic acid (MA) displays anti-tumor function in various types of cancers by

Maslinic acid induces mitochondrial apoptosis and suppresses HIF-1α expression in A549 lung cancer cells under normoxic and hypoxic conditions.

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The apoptotic effects of maslinic acid (MA) at 4, 8, 16, 32 and 64 μmol/L on human lung cancer A549 cells under normoxic and hypoxic conditions were examined. MA at 4-64 and 16-64 μmol/L lowered Bcl-2 expression under normoxic and hypoxic conditions, respectively (p < 0.05). This agent at 4-64

Maslinic acid potentiates the anti-tumor activity of tumor necrosis factor alpha by inhibiting NF-kappaB signaling pathway.

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BACKGROUND Tumor necrosis factor alpha (TNFalpha) has been used to treat certain tumors in clinic trials. However, the curative effect of TNFalpha has been undermined by the induced-NF-kappaB activation in many types of tumor. Maslinic acid (MA), a pharmacological safe natural product, has been

Effects of maslinic acid on the proliferation and apoptosis of A549 lung cancer cells.

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Maslinic acid (MA) is a pentacyclic triterpene acid that is present in numerous dietary plants. Although certain studies have demonstrated that MA has anti‑cancer properties in different cell types, the effect of MA on lung cancer cell proliferation and apoptosis and the potential underlying

Maslinic acid potentiates the antitumor activities of gemcitabine in vitro and in vivo by inhibiting NF-κB-mediated survival signaling pathways in human gallbladder cancer cells.

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Gemcitabine (GEM) is one of the first-line drugs in the treatment of gallbladder cancer (GBC), although the therapeutic effect is not sustained due to resistance to the drug over time. Maslinic acid (MA) has been shown to inhibit transcription factor nuclear factor-κB (NF-κB), resulting in the

Esters and amides of maslinic acid trigger apoptosis in human tumor cells and alter their mode of action with respect to the substitution pattern at C-28.

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Cancer is one of the most commonly diagnosed diseases worldwide; its mortality rate is high, and there is still a demand for the development of antitumor active drugs. Triterpenoic acids show many pharmacological effects, among them antitumor activity. One of these, maslinic acid-1 is of interest

Maslinic acid differentially exploits the MAPK pathway in estrogen-positive and triple-negative breast cancer to induce mitochondrion-mediated, caspase-independent apoptosis

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Breast cancer accounts for 1.4 million new cases every year. Triple-negative breast cancer (TNBC) is one the leading cause of mortality in developing countries and is associated with early age onset (under 40 years old). Chemotherapy has a poor success rate in patients with TNBC as compared to other

3D-QSAR studies on Maslinic acid analogs for Anticancer activity against Breast Cancer cell line MCF-7.

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Global prevalence of breast cancer and its rising frequency makes it a key area of research in drug discovery programs. The research article describes the development of field based 3D-QSAR model based on human breast cancer cell line MCF7 in vitro anticancer activity, which defines the molecular

The natural triterpene maslinic acid induces apoptosis in HT29 colon cancer cells by a JNK-p53-dependent mechanism.

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BACKGROUND Maslinic acid, a pentacyclic triterpene found in the protective wax-like coating of the leaves and fruit of Olea europaea L., is a promising agent for the prevention of colon cancer. We have shown elsewhere that maslinic acid inhibits cell proliferation to a significant extent and

Cancer chemopreventive activity of maslinic acid: suppression of COX-2 expression and inhibition of NF-κB and AP-1 activation in Raji cells.

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Chronic inflammation is one of the predisposing factors for neoplastic transformation. Targeting inflammation through suppression of the pro-inflammatory pathway by dietary phytochemicals provides an important strategy for cancer prevention. Maslinic acid is a novel natural triterpenoid known to

Maslinic acid, a triterpenic anti-tumoural agent, interferes with cytoskeleton protein expression in HT29 human colon-cancer cells.

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Maslinic acid (MA) is an anti-tumoural agent which shows potent anti-proliferative properties against the HT29 colon-cancer cells. To shed light upon the active mechanism of MA we have investigated its effects upon the cytoskeleton. We used a proteomics procedure based on two-dimensional gel

Maslinic acid and its in vitro anti-neoplastic effects.

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Maslinic acid promotes autophagy by disrupting the interaction between Bcl2 and Beclin1 in rat pheochromocytoma PC12 cells.

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Maslinic acid (2α, 3β-dihydroxyolean-12-en-28-oic acid, MA) was isolated from natural plants and showed anti-cancer activity in rat Pheochromocytoma PC12 cells in our previous studies. We now discover that MA disrupts the interaction between Bcl2 and autophagy scaffold protein Beclin1 in the above

Targeting inflammatory pathways by triterpenoids for prevention and treatment of cancer.

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Traditional medicine and diet has served mankind through the ages for prevention and treatment of most chronic diseases. Mounting evidence suggests that chronic inflammation mediates most chronic diseases, including cancer. More than other transcription factors, nuclear factor-kappaB (NF-κB) and

Screening of plant constituents for effect on glucose transport activity in Ehrlich ascites tumour cells.

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The effect of plant extracts on D-glucose uptake by Ehrlich ascites tumour cells was examined. Among the 23 extracts of medicinal plants, five samples inhibited, and six samples activated, the uptake significantly. From one of the active plants, Lagerstroemia speciosa, two triterpenoids, colosolic

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