Copper metabolism in Saccharomyces cerevisiae: an update.

Copper is an essential element in all forms of life. It acts as a cofactor of some enzymes and is involved in forming proper protein conformations. However, excess copper ions in cells are detrimental as they can generate free radicals or disrupt protein structures.

Nanoparticle-Encapsulated Liushenwan Could Treat Nanodiethylnitrosamine-Induced Liver Cancer in Mice by Interfering With Multiple Critical Factors for the Tumor Microenvironment.

We previously isolated an ethanol fraction of LSW (Liushenwan pill, a traditional Chinese medicine) which has been shown to prevent and treat liver cancer induced by nanodiethylnitrosamine (nanoDEN) in mice. In the present study, we utilized a high-pressure microfluidics technique to generate LSW lipid nanoparticles (nano-LSW) to reduce its toxicity, and enhance its inhibitory effect on tumor growth, and further evaluate its therapeutic effect using a nanoDEN-induced mouse model of liver cancer. Our results indicated that nano-LSW-low could induce apoptosis in HepG2 cells, but exhibited low toxicity in L02 cells.

The molecular mechanisms of copper metabolism and its roles in human diseases.

Copper is an essential element in cells; it can act as either a recipient or a donor of electrons, participating in various reactions. However, an excess of copper ions in cells is detrimental as these copper ions can generate free radicals and increase oxidative stress. In multicellular organisms, copper metabolism involves uptake, distribution, sequestration, and excretion, at both the cellular and systemic levels.

ΔNp63α down-regulates c-Myc modulator MM1 via E3 ligase HERC3 in the regulation of cell senescence.

p63 and c-Myc are key transcription factors controlling genes involved in the cell cycle and cellular senescence. We previously reported that p63α can destabilize MM1 protein to derepress c-Myc, resulting in cell cycle progress and tumorigenesis. However, how the proteasomal degradation of MM1 is facilitated remains unclear.

Cullin3/KCTD5 induces monoubiquitination of ΔNp63α and impairs its activity.

Potassium channel tetramerization domain containing 5 (KCTD5) was previously documented as a component of the Cullin3-RING ligase (CRL3). It has been reported that KCTD5 can induce enrichment of polyubiquitinated proteins, and KCTD5-based CRL3 destabilizes several proteins. In our present study, we report that KCTD5 may physically interact with ΔNp63α, which is a member of the p53 family.

A double dealing tale of p63: an oncogene or a tumor suppressor.

As a member of tumor suppressor p53 family, p63, a gene encoding versatile protein variant, has been documented to correlate with cancer formation and progression, though it is rarely mutated in cancer patients. However, it has long been controversial on whether p63 is an oncogene or a tumor suppressor. Here, we comprehensively reviewed reports on roles of p63 in development, tumorigenesis and tumor progression.

[Effect of PI3K/AKT inhibitor on benign prostate hyperplasia and its mechanism: an experimental study].

Objective: To explore the effect of the phosphoinositide 3-kinase/protein kinase B (PI3K/PKB or PI3K/AKT) signaling pathway inhibitor on benign prostate hyperplasia (BPH) and its mechanism.

Methods: Forty-eight SD male adult rats aged 12 weeks were equally randomized to 4 groups: sham operation control, BPH model, 50 mg LY294002 and 100 mg LY294002. The BPH models were made by muscular injection of testosterone propionate at 10 mg/kg/d for 30 days following castration.

[Cytogenetic analysis and phenotype location analysis on the karyotype of a ring chromosome 21 syndrome].

Objective: To search the forming cause and the correlation between the clinical phenotype and chromosome band by the cytogenetic analysis on a case of ring chromosome 21 syndrome.

Methods: Identification and location of 21 ring chromosome were performed with the G-banding, C-banding, N-banding, high-resolution banding and fluorescence in situ hybridization (FISH) techniques.

Results: It was found that the karyotypes of the patient's parents are normal.