Low-dose adropin stimulates inflammasome activation of macrophage via mitochondrial ROS involved in colorectal cancer progression.

Adropin is encoded by the energy homeostasis-associated (ENHO) gene and widely present in liver, pancreas, heart, kidney, brain, and vascular tissues. Abnormal adropin is associated with metabolic, inflammatory, immune, and central nervous disorders. Whether adropin is involved in the development of colorectal cancer (CRC) is still unclear. Here, decreased adropin expression of tumor-nest cells in advanced-stage CRC was demonstrated. Adropin expressed by carcinoma cells was negatively correlated with macrophage infiltration in the matrix of CRC tissues. However, tumor macrophages enhanced adropin expression and were positively correlated with tumor invasion and metastasis. ENHO gene transfection into colon cancer (MC38) cells inhibited tumor growth in vivo, accompanying the increase of M1 macrophages. Treatment with low-dose adropin (< 100 ng/mL) on macrophages ex vivo directly increased mitochondrial reactive oxygen species for inflammasome activation. Furthermore, ENHO-/- mice had less M1 macrophages in vivo, and ENHO-/- macrophages were inert to be induced into the M1 subset ex vivo. Finally, low-dose adropin promoted glucose utilization, and high-dose adropin enhanced the expression of CPT1α in macrophages. Therefore, variations of adropin level in carcinoma cells or macrophages in tumor tissues are differently involved in CRC progression. Low-dose adropin stimulates the antitumor activity of macrophages, but high-dose adropin facilitates the pro-tumor activity of macrophages. Increasing or decreasing the adropin level can inhibit tumor progression at different CRC stages.

15-Methacryloyloxypentadecyl Dihydrogen Phosphate Improves Resin-to-Zirconia Bonding Durability.

PURPOSE: To investigate the bond durability of composite cement to zirconia after treatment with a 15-methacryloyloxypentadecyl dihydrogen phosphate (15-MPDP)-containing adhesive and 2 commercially available adhesives. MATERIALS AND METHODS: Ninety zirconia bars were fabricated and bonded to prepolymerized resin composite cylinders with a composite cement after surface treatment for 20 s using the following adhesives: Adper Easy One (AEO, negative control), Single Bond Universal (SBU, positive control), and 10 wt% 15-MPDP powder mixed with Adper Easy One (15- MPDP). After storage in distilled water at 37°C for 24 h, the specimens were divided into 3 subgroups according to the aging treatment applied (n = 10): no aging treatment (0/TC), 10,000 thermocycles (1/TC), and 37,500 thermocycles (3/TC). Shear bond strength (SBS) was analyzed using two-way ANOVA (p < 0.05), and the fracture surfaces were examined under a dental microscope. RESULTS: Significant differences in the SBSs among the surface treatments and aging treatments were observed (both p < 0.001). The 15-MPDP and SBU groups showed significantly higher SBSs than the AEO group, whereas similar SBSs were found in the 15-MPDP and SBU groups. Significant reductions in the SBSs were found after 37,500 thermocycles (p < 0.001), although no significant difference between specimens aged with 10,000 thermocycles and non-aged specimens was observed. CONCLUSIONS: The 15-MPDP-containing dental adhesive exhibited bond durability comparable to that of a well-established 10-MDP-containing universal adhesive. Aging by 10,000 thermocycles may be insufficient to disrupt the bond of composite cement to zirconia.

MicroRNA-28-5p as a potential diagnostic biomarker for chronic periodontitis and its role in cell proliferation and inflammatory response.

Background/purpose: Recent studies have pointed to the crucial role of microRNAs (miRNAs) in chronic periodontitis (CP). This study investigated the regulation and potential mechanisms of miR-28-5p in CP patients and lipopolysaccharide (LPS)-induced periodontal ligament cells (PDLCs). Materials and methods: 76 CP patients and 71 periodontally healthy subjects were included. RT-qPCR was employed to examine miR-28-5p and sphingosine kinase -1 (SPHK1) in subjects' gingival sulcus fluid and PDLCs. The diagnostic performance was evaluated by measuring the area under the curve (AUC) of the receiver operating characteristic (ROC) analysis. Pearson correlation coefficient (r) was adopted to explore the statistical relation between indicators. PDLCs proliferation and inflammation factors were determined by CCK-8 and ELISA assay. The direct target gene was validated by a dual-luciferase reporter assay. Results: miR-28-5p was lowly expressed in CP patients and LPS-induced PDLCs (P < 0.05). AUC for miR-28-5p was 0.937, which had certain diagnostic value. Additionally, miR-28-5p was negatively correlated with periodontal clinical indicators and inflammatory factors. Cell proliferation of PDLCs was inhibited and inflammation was promoted under LPS induction, however, elevated miR-28-5p diminished the effect of LPS (P < 0.05). SPHK1 acts as a miR-28-5p target and the elevation of SPHK1 caused by LPS treatment was inhibited by the increased miR-28-5p. Conclusion: Present study revealed that miR-28-5p could be served as a potential diagnostic biomarker for CP. And miR-28-5p may participate in CP progression by targeting SPHK1 to regulate the proliferation and inflammation of PDLCs. This study may offer insights into CP treatment and diagnosis.

CircPUM1 Knockdown Confers Radiosensitivity in Oral Squamous Cell Carcinoma by Regulating the miR-580/STAT3 Pathway.

Background: CircPUM1 acts as an oncogene in a variety of tumors, and there is no related research on oral squamous cell carcinoma. This study aimed to evaluate the clinical significance of CircPUM1 in oral squamous cell carcinoma radiotherapy. Methods: Radio-resistant cell lines were established by increasing the X-ray dose. Analysis of CircPUM1 expression in oral squamous cell carcinoma was carried out using bioinformatics tools. Cell proliferation was analyzed with CCK-8 and colony formation. Protein and gene expressions were detected by Western blotting and qPCR. RNA interference inhibits endogenous gene expression. A luciferase reporter system and immunoprecipitation were used to validate the target of CircPUM1. Result: CircPUM1 was highly expressed in OSCC. The higher the expression level of CircPUM1 in OSCC, the worse the clinical features and prognosis. Knockdown of CircPUM1 enhances the sensitivity of OSCC cells to X-rays, and expression of exogenous CircPUM1 makes OSCC cells acquire radiation resistance. The absence of CircPUM1 blocked the cells in the G0/G1 phase and triggered apoptosis. The prediction of mir-580-binding site, luciferase reporter system, and immunoprecipitation confirmed that mir-580 is the binding site of CircPUM1. In addition, STAT3 was predicted and confirmed as the binding site of mir-580. Overexpression of STAT3 partially attenuated the radiosensitivity of OSCC cells to knockdown of CircPUM1. Conclusion: CircPUM1 has the oncogene expression profile in oral squamous cell carcinoma; patients with high expression of CircPUM1 have less benefit from radiotherapy and need more frequent follow-up. In addition, CircPUM1 may be a potential therapeutic target for oral squamous cell carcinoma. The CircPUM1/mir-580/STAT3 axis has a certain effect on the radiosensitivity of OSCC. These results suggest that patients with low expression of CircPUM1 may gain more benefits.

Dual-wavelength distributed feedback fiber laser based on double exposure and equivalent phase shift method.

A special sampling structure based on double exposure technology is proposed to achieve dual-wavelength lasing in the distributed feedback fiber laser. This structure is composed of two grating pitches in one sampling period, which could be realized by changing the fiber's length in the fabrication. Through employing an equivalent phase shift, only a submicrometer-level precision is required for precise phase control. Then a stable dual-wavelength laser with the spacing of 400 pm is obtained in the experiment successfully. The output power is 30.46 µW and the sidemode suppression ratio is 46 dB under a pumped power of 146 mW.