Heterochromatin protein 1 (HP1) is an epigenetic modifier of gene regulation and chromatin packing via binding to trimethylated histone H3 lysine 9 (H3K9). HP1 plays an important role in gene activation as well as gene repression in heterochromatin and euchromatin. However, the role of individual HP1 proteins in human diseases remains elusive. Here, we show that HP1β negatively regulates the expression and activation of matrix metallopeptidase (MMP)2, which mediates cancer metastasis by destructing type Ⅳ collagen. Reduced HP1β expression correlates with the increased level of pro- and active-MMP2 in colon cancer cells. Consistently, HP1β knockdown (KD) increased and HP1β overexpression decreased the mRNA level of MMP2 and membrane type 1 metallopeptidase (MT1-MMP). Furthermore, cancer cells overexpressing HP1β showed impaired migratory ability, whereas HP1β‑deleted cancer cells had increased migration. HP1β negatively regulates MMP2 expression in a transcriptional level and prevents MMP2 activation through reducing the expression of MT1‑MMP. These findings shed new light on HP1β as a molecular regulator and an efficient therapeutic target of metastatic cancer.
Objectives: This study investigated the effect of infection control barrier thickness on power density, wavelength, and light diffusion of light curing units. Materials and Methods: Infection control barrier (Cleanwrap) in one-fold, two-fold, four-fold, and eightfold, and a halogen light curing unit (Optilux 360) and a light emitting diode (LED) light curing unit (Elipar FreeLight 2) were used in this study. Power density of light curing units with infection control barriers covering the fiberoptic bundle was measured with a hand held dental radiometer (Cure Rite). Wavelength of light curing units fixed on a custom made optical breadboard was measured with a portable spectroradiometer (CS-1000). Light diffusion of light curing units was photographed with DSLR (Nikon D70s) as above. Results: Power density decreased significantly as the layer thickness of the infection control barrier increased, except the one-fold and two-fold in halogen light curing unit. Especially, when the barrier was four-fold and more in the halogen light curing unit, the decrease of power density was more prominent. The wavelength of light curing units was not affected by the barriers and almost no change was detected in the peak wavelength. Light diffusion of LED light curing unit was not affected by barriers, however, halogen light curing unit showed decrease in light diffusion angle when the barrier was four-fold and statistically different decrease when the barrier was eight-fold (p < 0.05). Conclusions: It could be assumed that the infection control barriers should be used as two-fold rather than one-fold to prevent tearing of the barriers and subsequent cross contamination between the patients. [J Kor Acad Cons Dent 2010;35(5):368-373.]
Nonselective histone deacetylase (HDAC) inhibitors have therapeutic effects, but exhibit dose-limiting toxicities in patients with multiple myeloma (MM). The present study investigated the interaction between the HDAC6 inhibitor, A452, and immunomodulatory drugs (IMiDs) on dexamethasone (Dex)-sensitive and -resistant MM cells compared with the current clinically tested HDAC6 inhibitor, ACY-1215. It was shown that the combination of the HDAC6-selective inhibitor, A452, with either of the IMiDs tested (lenalidomide or pomalidomide) led to the synergistic inhibition of cell growth, a decrease in the viability of MM cells and in an increase in the levels of apoptosis. Furthermore, enhanced cell death was associated with the inactivation of AKT and extracellular signal-regulated kinase (ERK)1/2. Of note, A452 in combination with IMiDs induced synergistic MM cytotoxicity without altering the expression of cereblon and thereby, the synergistic downregulation of IKAROS family zinc finger (IKZF)1/3, c-Myc and interferon regulatory factor 4 (IRF4). Furthermore, combined treatment with A452 and IMiDs induced the synergistic upregulation of PD-L1. More importantly, this combination treatment was effective in the Dex-resistant MM cells. Overall, the findings of this study indicate that A452 is more effective as an anticancer agent than ACY-1215. Taken together, these findings suggest that a combination of the HDAC6-selective inhibitor, A452, and IMiDs may prove to be beneficial in the treatment of patients with MM.
The purpose of this study was to compare the sealing abilities of four endodontic temporary restorative materials using a methylene blue dye penetration test under dynamic loading. Standardized access cavities were prepared in forty-four intact human permanent molar teeth, and the cavities were restored with Caviton, MD-Temp, IRM, or ZOE. After thermocycling, an intermittent load of 98 N at 1 Hz was applied for 1,000 cycles to the long axis of the functional cusp of each of the teeth, which were immersed in a 1% methylene blue solution. The teeth were split in half, and the linear depth of dye penetration was evaluated according to the criteria. The results were analyzed using one-way ANOVA (p = 0.05) and Duncan' s multiple range test. The results demonstrated that Caviton and MD-Temp showed significantly lower microleakage than IRM and ZOE. It was concluded that Caviton and MD-Temp exhibited better sealing ability than IRM and ZOE under dynamic loading. [J Kor Acad Cons Dent 33(3):198-203, 2008]
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