Gain-of-function p53 mutant with 21-bp deletion confers susceptibility to multidrug resistance in MCF-7 cells.

The majority of p53 mutations, which are responsible for gain of oncogenic function, are missense mutations in hotspot codons. However, in our previous study, we demonstrated that a deletion spanning codons 127-133 in the p53 gene (designated as del p53) was detected in doxorubicin-resistant MCF-7 cell lines following various induction processes. In the present study, we aimed to investigate the role of del p53 and its association with the proliferation, metastasis and drug resistance of MCF-7 cells.

A critical dose of doxorubicin is required to alter the gene expression profiles in MCF-7 cells acquiring multidrug resistance.

Cellular mechanisms of multidrug resistance (MDR) are related to ABC transporters, apoptosis, antioxidation, drug metabolism, DNA repair and cell proliferation. It remains unclear whether the process of resistance development is programmable. We aimed to study gene expression profiling circumstances in MCF-7 during MDR development.

Cytotoxicity and reversal of multidrug resistance by tryptanthrin-derived indoloquinazolines.

Aim: To evaluate the effects and elucidate the mechanisms of a series of indoloquinazolines as novel anticancer agents.

Methods: Condensation of the substituted isatoic anhydride with the substituted isatin was performed to prepare compounds 1-4, followed by adding malononitrile to prepare compounds 5-7. Cytotoxicity was measured by MTT assays.

Downregulation of GSTpi expression by tryptanthrin contributing to sensitization of doxorubicin-resistant MCF-7 cells through c-jun NH2-terminal kinase-mediated apoptosis.

Overexpression of GSTpi and underexpression of Topo II expression are associated with multidrug resistance (MDR) phenotype through nontransporter pathway. Tryptanthrin, a quinazoline derivative, was reported to sensitize resistant cells to doxorubicin by downregulation of MDR1 expression. This study aims to extendedly investigate the effect of tryptanthrin on the role of nontransporter-based genes in determining the MDR response in doxorubicin-resistant MCF-7 cells (MCF-7/adr).

Apoptosis and necrosis are involved in the toxicity of Sauropus androgynus in an in vitro study.

Background/purpose: The raw juice of the young sticks and leaves of Sauropus androgynus (SA) has been widely used as a natural food for body weight reduction and vision protection in Taiwan and Southeast Asia. But as has been reported, SA-associated obliterative bronchiolitis can develop after taking SA for more than 3 months. Lung transplantation was carried out in severe cases.

Olanzapine induces SREBP-1-related adipogenesis in 3T3-L1 cells.

Olanzapine is a second-generation atypical antipsychotic drug (AAPD). Major side effects of olanzapine are weight gain and development of diabetes mellitus, which are risk factors of cardiovascular diseases. The possible causes of metabolic adverse effects are known as poor satiety and increased food intake due to blockade of receptors such as 5-HT(2C) in CNS.

Tryptanthrin inhibits MDR1 and reverses doxorubicin resistance in breast cancer cells.

Development of agents to overcome multidrug resistance (MDR) is important in cancer chemotherapy. Up to date, few chemicals have been reported to down-regulate MDR1 gene expression. We evaluated the effect of tryptanthrin on P-glycoprotein (P-gp)-mediated MDR in a breast cancer cell line MCF-7.

3-O-beta-D-glucosyl-(1-->6)-beta-D-glucosyl-kaempferol isolated from Sauropus androgenus reduces body weight gain in Wistar rats.

The young sticks and leaves of Sauropus androgynus (SA) that had been used as a health food for body weight reduction, led to an outbreak of obliterative bronchiolitis in Taiwan. This study tested the toxicity and anti-obesity features of the SA-isolated compound, 3-O-beta-D-glucosyl-(1-->6)-beta-D-glucosyl-kaempferol (GGK), on male Wistar rats receiving 6 or 60 mg/kg of GGK orally as well as partial purified EtOAc and n-BuOH fractions of SA extract daily for 28 d. Sixty milligrams per kilogram GGK treatment significantly reduced food intake in rats by 15% (p<0.