LncRNA-cCSC1 promotes cell proliferation of colorectal cancer through sponging miR-124-3p and upregulating CD44.

LncRNA-cCSC1 is highly expressed in colorectal cancer (CRC). The study was designed to evaluate the function and mechanism of lncRNA-cCSC1 in cell proliferation of CRC. RT-PCR was used to measure the expression levels of lncRNA-cCSC1 in CRC cell lines. CCK-8, colony formation, EdU staining, flow cytometry and Western blot were performed to examine the effect of interference with lncRNA-cCSC1 expression on cell proliferation. miR-124-3p and the target genes of miR-124-3p were investigated using bioinformatics analysis and verified by dual-luciferase reporter, RT-PCR and Western blot. Rescue experiments were carried out to confirm the role of miR-124-3p in cell proliferation of CRC. Our results showed that cell proliferation of CRC was promoted by lncRNA-cCSC1 upregulation and inhibited by lncRNA-cCSC1 downregulation. In addition, miR-124-3p is predicted to be the target of lncRNA-cCSC1 and is negatively correlated with lncRNA-cCSC1. Moreover, the addition of miR-124-3p mimics or inhibitor reversed the effects induced by lncRNA-cCSC1 overexpression or silencing on cell proliferation of CRC. Additionally, lncRNA-cCSC1 regulated the expression level of CD44, a target gene of miR-124-3p. Finally, we studied the effects of the lncRNA-cCSC1/miR-124-3p axis on CD44. These results indicate that lncRNA-cCSC1 promotes cell proliferation of CRC through sponging miR-124-3p and upregulating CD44.

Low-Dose 4-Hydroxy-2-Nonenal (HNE) Reperfusion Therapy Displays Cardioprotective Effects in Mice After Myocardial Infarction That Are Abrogated by Genipin.

BACKGROUND Revascularization is a successful therapeutic strategy for myocardial infarction. However, restoring coronary blood flow can lead to ischemia-reperfusion (I/R) injury. Low-dose 4-hydroxy-2-nonenal (HNE) therapy appears to play a key role in myocardial tolerance to I/R injury. We hypothesized that the positive effects of HNE on myocardial I/R injury may be UCP3-dependent. MATERIAL AND METHODS Adult male wild-type (WT) or UCP3 knockout (UCP3-/-) mice were pre-treated with the UCP inhibitor genipin or saline 1 h before ischemia and underwent 30-min coronary artery ligation followed by 24-h reperfusion. Mice were treated with intravenous HNE (4 mg/kg) or saline 5 min before reperfusion. Echocardiography was conducted to measure left ventricular end-diastolic posterior wall thickness (LVPWd), end-diastolic diameter (LVEDD), and fractional shortening (FS). Infarct size was measured by TTC staining. qRT-PCR and Western blotting were used to assess the expression of UCP3, UCP2, and the apoptosis markers cytochrome C and cleaved caspase-3. RESULTS HNE improved survival at 24 h post-MI in wild-type mice (p<0.05) but not in UCP3-/- mice. HNE preserved LVEDD and FS in WT mice (p<0.05) but not in UCP3-/- mice. HNE reduced infarct size in WT mice (p<0.05) but not in UCP3-/- mice. HNE upregulated UCP3 expression (p<0.05) but did not affect UCP2 expression. HNE reduced apoptosis marker expression in WT mice (p<0.05) but not in UCP3-/- mice. HNE's positive effects were abrogated by genipin in an UCP3-dependent manner. CONCLUSIONS Low-dose HNE reperfusion therapy attenuates murine myocardial I/R injury in an UCP3-dependent manner. These effects are abrogated by genipin in an UCP3-dependent manner.

MR imaging features and a redefinition of the classification system for nodular fasciitis.

To analyze magnetic resonance imaging features of nodular fasciitis and redefine the system for classifying this class of lesions.Twenty-seven patients with nodular fasciitis and 71 patients with other soft tissue lesions who underwent surgery or biopsy were retrospectively analysed. Demographic information, medical history, and magnetic resonance imaging features were collected. Classification of nodular fasciitis was performed based on a redefined system. Comparison between 2 groups was performed with Chi-square or Fisher exact test.For nodular fasciitis, the longest average lesion diameter was 1.87 cm (range, 0.52-5.46 cm), and 40.7% of lesions were located in the upper extremities, while 29.6% were located in the head and neck. Compared with skeletal muscle, most lesions exhibited isointensity on T1-weighted imaging and hyperintensity on T2-weighted imaging, and 45.5% of the lesions exhibited rim enhancement, 40.9% showed obvious homogenous enhancement, while 13.6% showed no enhancement or slight enhancement. The subcutaneous type accounted for 25.9% of cases, the fascial type 25.9%, the intramuscular type 29.6%, and the unclassified type 18.5%. The "fascia tail sign" was more frequently observed in nodular fasciitis than in other soft tissue lesions (P < .001). Nodular fasciitis was slightly more likely to present with the "inverted target sign" and "solar halo sign" than other soft tissue lesions (P > .05). The "cloud sign" only appeared in nodular fasciitis (P < .05).The "fascia tail sign" and "cloud sign" could help differentiate nodular fasciitis from other soft tissue lesions. A new classification may improve understanding about nodular fasciitis.

TNAP inhibition attenuates cardiac fibrosis induced by myocardial infarction through deactivating TGF-ß1/Smads and activating P53 signaling pathways.

Tissue nonspecific alkaline phosphatase (TNAP) is expressed widely in different tissues, modulating functions of metabolism and inflammation. However, the effect of TNAP on cardiac fibrosis remains controversial and needs to be further studied. The present study aims to investigate the role of TNAP on myocardial infarction (MI)-induced fibrosis and its mechanism. TNAP was upregulated in patients with MI, both in serum and injured hearts, and predicted in-hospital mortality. TNAP was also significantly upregulated after MI in rats, mostly in the border zone of the infarcted hearts combined with collagen synthesis. Administration of TNAP inhibitor, tetramisole, markedly improved cardiac function and fibrosis after MI. In the primary cultures of neonatal rat cardiac fibroblasts (CFs), TNAP inhibition significantly attenuated migration, differentiation, and expression of collagen-related genes. The TGF-ß1/Smads signaling suppression, and p-AMPK and p53 upregulation were involved in the process. When p53 inhibitor was administered, the antifibrotic effect of TNAP inhibition can be blocked. This study provides a direct evidence that inhibition of TNAP might be a novel regulator in cardiac fibrosis and exert an antifibrotic effect mainly through AMPK-TGF-ß1/Smads and p53 signals.