Bio‑informatics analysis of renal carcinoma gene matrix metalloproteinase‑7.

BACKGROUND: Renal cancer is one of the common malignant tumors of the urinary system, seriously threatening human being’s health. The current discoveries, however, are far enough for efficient and secure treatment of renal cancer. AIMS: The aim was to explore the mechanism of matrix metalloproteinase‑7 (MMP‑7) protein in renal carcinoma cell metastasis by bioinformatics analysis. MATERIALS AND METHODS: Bioinformatics methods were used to analyze the composition of amino acids, as well as transmembrane structure, coiled coils, subcellular localization, signal peptide, functions and structures at all levels. RESULTS AND CONCLUSIONS: It showed that the gene MMP‑7 totally had 1131 bp. A peptide chain containing 267 amino acids was encoded in the coding region. Based on random coil, α helix, and further super‑helix, it had formed a stable neutral hydrophilic protein. The subcellular location analysis indicated that the protein was located outside the cell. The mature peptide started from the 18th amino acid, and its front‑end was the sequence of the signal peptide, belonging to the secreted protein. Analysis of the functional domain showed that this protein had two functional domains, the PG binding domain, and the zinc finger binding domain. Moreover, the protein, which was cross‑linked with it, was also one related to cancer cell proliferation and metastasis. To sum up, MMP‑7 is a stable neutral hydrophilic secreted protein, and it may play a vital role in the invasion and metastasis of cancer cells.

Histone demethylase retinoblastoma binding protein 2 regulates the expression of -smooth muscle actin and vimentin in cirrhotic livers

Liver cirrhosis is one of the most common diseases of Chinese patients. Herein, we report the high expression of a newly identified histone 3 lysine 4 demethylase, retinoblastoma binding protein 2 (RBP2), and its role in liver cirrhosis in humans. The siRNA knockdown of RBP2 expression in hepatic stellate cells (HSCs) reduced levels of α-smooth muscle actin (α-SMA) and vimentin and decreased the proliferation of HSCs; and overexpression of RBP2 increased α-SMA and vimentin levels. Treatment with transforming growth factor β (TGF-β) upregulated the expression of RBP2, α-SMA, and vimentin, and the siRNA knockdown of RBP2 expression attenuated TGF-β-mediated upregulation of α-SMA and vimentin expression and HSC proliferation. Furthermore, RBP2 was highly expressed in cirrhotic rat livers. Therefore, RBP2 may participate in the pathogenesis of liver cirrhosis by regulating the expression of α-SMA and vimentin. RBP2 may be a useful marker for the diagnosis and treatment of liver cirrhosis.

Effect of curcumin on the proliferation and apoptosis of hepatic stellate cells

This study was designed to investigate the effect of curcumin (diferuloylmethane) on the proliferation and apoptosis of hepatic stellate cells (HSC). The cell line HSC-T6 (1.25 x 10(5) cells/mL) was incubated with curcumin and HSC proliferation was detected by a methyl thiazolyl tetrazolium colorimetric assay. HSC apoptosis was detected by flow cytometry, transmission electron microscope and agarose gel electrophoresis. HSC proliferation was significantly inhibited in a concentration-dependent manner (10.6 to 63.5 percent) after incubation with 20-100 ìM curcumin, compared with a control group. At 20, 40, and 60 ìM, after 24 h of incubation, curcumin was associated with a significant increase in the number of HSC in the G2/M phase, and a significant decrease in cell numbers in the S phase (P < 0.05). At these concentrations, curcumin was also associated with an increase in the apoptosis index of 15.3 ± 1.9, 26.7 ± 2.8, and 37.6 ± 4.4 percent, respectively, compared to control (1.9 ± 0.6 percent, P < 0.01). At 40 ìM, the curcumin-induced apoptosis index at 12, 24, 36, and 48 h of incubation was 12.0 ± 2.4, 26.7 ± 3.5, 33.8 ± 1.8, and 49.3 ± 1.6 percent, respectively (P < 0.01). In conclusion, curcumin inhibits the in vitro proliferation of HSCs in the G2/M phase of the cell cycle and also induces apoptosis in a concentration- and time-dependent manner. The in vivo effect of curcumin on HSCs requires further investigation.

Role of left cardiac sympathetic denervation in the management of congenital long QT syndrome.

Congenital long QT syndrome (LQTS) is a rare but life-threatening disorder affecting cardiac electrophysiology. It occurs due to mutation in genes encoding for the ion channels in ventricular cell membrane. Syncopal attacks and cardiac arrest are the main symptoms of the disease. Anti-adrenergic therapy with oral beta-blockers has been the mainstay of treatment for LQTS. However, up to 30% of patients fail to respond to medical therapy and remain symptomatic. An alarming 10% of patients still experience cardiac arrest or sudden cardiac death during the course of therapy. Left cardiac sympathetic denervation (LCSD) has been used as an alternative therapy in patients who are resistant to beta-blockers. Although LCSD appears effective in reducing the frequency of syncopal attacks and improving the survival rate in both the short and long-term, its use has not gained popularity. The recent advent of minimally invasive thoracoscopic sympathectomy may improve the acceptance of LCSD by physicians and patients in the future. The primary objective of this article was to review the current evidence of the clinical efficacy and safety of LCSD in the management of LQTS. The review was based on Medline search of articles published between 1966 and 2002.