CircRNA_101237 promotes NSCLC progression via the miRNA-490-3p/MAPK1 axis.

Non-small cell lung cancer (NSCLC) is a common type of lung cancer, characterized by a poor prognosis. In the last several years, more and more studies have demonstrated the significant roles played by circular RNAs (circRNAs) in different human tumors progression including NSCLC. The present study was to explore the mechanism of hsa_circ_101237 in regulating non-small cell lung cancer (NSCLC). Totally 303 NSCLC cases were enrolled. A549 and H1299 cells were transfected. Cells viability, migration and invasion were determined by CCK-8 assay and transwell experiment, respectively. Luciferase reporter gene assay and RNA immunoprecipitation (RIP) assay were performed. hsa_circ_101237, miR-490-3p and MAPK1 expression in tissues/cells were detected by qRT-PCR. The study found an elevation in the expression of Hsa_circRNA_101237 in both NSCLC tissues and cell line. High Hsa_circRNA_101237 expression predicted poor survival in NSCLC. Meanwhile, we found that hsa_circRNA_101237 expression sponged miR-490-3p to enhance MAPK1 expression, thus significantly promoting NSCLC cell lines proliferation, migration, and invasion. MAPK1 restoration prevented NSCLC cells proliferation, migration, and invasion to be repressed due to hsa_circRNA_101237 knockdown. To sum up, as revealed by the study, hsa_circRNA_101237 promoted the expression of MAPK1 via miRNA-490-3p sponge, thus affecting the NSCLC as an important onco-circRNA.

[Effect and mechanism of astragaloside â £ on Toll-like receptor pathway in fibrotic mice after renal ischemia-reperfusion].

The aim of this paper is to study the effect of astragaloside Ⅳ on renal fibrosis mice with ischemia-reperfusion injury (IRI) and discuss the mechanism. Male C57BL/6 50 mice were randomly divided into four groups, namely Sham-operated group, model group, AS-Ⅳ prevention group and AS-Ⅳ treatment group. Since the day of surgery, the mice in astragaloside Ⅳ prevention group were treated with astragaloside Ⅳ by gavage for 30 days at the dose of 30 mg·kg⁻¹·d⁻¹. At the 60th day after surgery, the mice in astragaloside Ⅳ treatment group were treated with astragaloside Ⅳ 100 by gavage for 30 days at the dose of 30 mg·kg⁻¹·d⁻¹. The mice in Sham-operated group and model group were treated with double distilled water containing 0.1% ethanol instead of astragaloside Ⅳ. Serum creatinine and blood urea nitrogen were detected by chemical methods. Histopathological changes and collagen deposition of affected kidneys were observed under optical microscope by HE and Masson staining. The expression levels of Toll like receptor pathway related molecules (TLR4,MyD88,TRAF6,TRAM,TRIF,NF-κB,TNF-α,IL-6, IFN-γ) in affected kidneys were observed by immunohistochemistry, Western blot methods and reverse transcription-PCR atprotein and mRNA levels in each group. The results showed that the degrees of fibrosis and histopathological damage of affected kidneys of mice in model group were the most obvious. And the expression levels of TLR4/MyD88 dependent signaling pathway-related molecules (TLR4 and MyD88, TRAF6 and NF-κB) in affected kidneys of mice in model group were the highest. At the same time, there was no difference in the expression levels of TLR4/MyD88 independent signaling pathway-related molecules（TRAM, TRIF）among sham-operated group, model group, astragaloside IV prevention group and astragaloside Ⅳ treatment group. In astragaloside Ⅳ prevention group and astragaloside Ⅳ treatment group, the injury of affected kidney was obviously reduced, and the protein expression levels of TLR4/MyD88 dependent signaling pathway-related molecules were also correspondingly reduced; at the same time, the expressions of terminal inflammatory cytokines (TNF-α,IL-6, IFN-γ) were suppressed. Therefore, astragaloside Ⅳ may improve renal interstitial fibrosis in mice after IRI by inhibiting the expression of TLR4/MyD88 dependent signaling pathway and the release of inflammatory cytokines (TNF-α,IL-6, IFN-γ), while the TLR4/MyD88 independent signaling pathway may not be involved in the process of renal fibrosis after ischemia-reperfusion injury.

The application value of capsule endoscopy in diagnosing small intestinal carcinoma.

OBJECTIVE: The aim of this study was to explore the clinical value of capsule endoscopy in the diagnosis of small intestine neoplastic lesions. MATERIALS AND METHODS: A retrospective analysis was conducted on the clinical data of 108 patients who underwent capsule endoscopic examination in the Endoscopy Center of Xinxiang Central Hospital from February 2010 to January 2014. The characteristics of different small bowel diseases were observed, and the prevalence rates of different small bowel lesions were calculated. RESULTS: Of the included 108 patients who received capsule endoscopic examination, 74 cases showed lesions, with a detection rate of 68.52%. Of these 74 patients, 56 cases (51.85%) suffered from small bowel diseases and 18 cases (16.67%) were manifested with other gastrointestinal lesions. Moreover, obvious lesion was not observed in 34 cases (31.48%). Among the patients with lesions, we observed seven cases of submucosal tumor in small intestines, five cases of small intestinal carcinoma, two cases of small intestinal polyps, two cases of small intestinal roundworm, eight cases of small intestine ulcer, one case of Crohn's disease, 18 cases of enteritis, two cases of small intestine diverticula, four cases of small intestine hemangioma, one case of small intestine vascular malformation, one case of intestinal lymphangiectasia, one case of small intestine compression, two cases of small intestine hemorrhage, and two cases of small intestinal lipoma. Among the patients who showed other gastrointestinal lesions, we observed one case of esophageal diverticula, three cases of gastric erosion, six cases of superficial gastritis, four cases of gastric ulcer, one case of pyloric ulcer, one case of colonic polyps, and two cases of colon tumor. CONCLUSION: Capsule endoscopy demonstrated a high diagnostic value for various small bowel diseases, including both tumor and inflammatory lesions. Given its simplicity, safety, and reliability, capsule endoscopy was an important examination tool for the diagnosis of small bowel diseases.

Recombinant Human Granulocyte Colony-Stimulating Factor Promotes Preinvasive and Invasive Estrogen Receptor-Positive Tumor Development in MMTV-erbB2 Mice.

PURPOSE: We investigated whether recombinant human granulocyte colony-stimulating factor (rhG-CSF) could promote the development of preinvasive and invasive breast cancer in mouse mammary tumor virus (MMTV-erbB2) mice with estrogen receptor-positive tumors. METHODS: MMTV-erbB2 mice were randomly divided into three experimental groups with 20 mice in each group. MMTV-erbB2 mice were treated with daily subcutaneous injections of vehicle or rhG-CSF (low-rhG-CSF group, rhG-CSF 0.125 µg; vehicle-rhG-CSF group, normal saline 0.25 µg; and high-rhG-CSF group, rhG-CSF 0.25 µg) at 3 months of age. Cellular and molecular mechanisms of G-CSF action in mammary glands were investigated via immunohistochemistry and reverse transcription polymerase chain reaction. RESULTS: Low, but not high, rhG-CSF doses significantly accelerated mammary tumorigenesis in MMTV-erbB2 mice. Short-term treatment with rhG-CSF could significantly promote the development of preinvasive mammary lesions. The cancer prevention effect was associated with reduced expression of proliferating cell nuclear antigen, cluster of differentiation 34, and signal transducers and activators of transcription 3 in mammary glands by >80%. CONCLUSION: We found that G-CSF was regulated by rhG-CSF both in vitro and in vivo. Identification of G-CSF genes helped us further understand the mechanism by which G-CSF promotes cancer. Low doses of rhG-CSF could significantly increase tumor latency and increase tumor multiplicity and burden. Moreover, rhG-CSF effectively promotes development of both malignant and premalignant mammary lesions in MMTV-erbB2 mice.

Silencing of COX-2 by RNAi modulates epithelial-mesenchymal transition in breast cancer cells partially dependent on the PGE2 cascade.

In order to prove whether downregulation of COX-2 (Cyclooxygenase-2) could modulate the epithelial- mesenchymal transition (EMT) of breast cancer, celecoxib and siRNA were respectively used to inhibit COX-2 function and expression in MDA-MB-231 cells. The EMT reversal effect in the RNAi treated group was better than that of the celecoxib group while there were no obvious differences in the medium PGE2 levels between the two groups. The results show that COX-2 pathways may contribute considerably to EMT of breast cancer cells, partially dependent on the PGE2 cascade. Akt2, ZEB2 and Snail were measured to clarify the underlying mechanisms of COX-2 on EMT; COX-2 may modulate EMT of breast cancer by regulating these factors. This finding may be helpful to elucidate the mechanisms of selective COX-2 inhibitor action in EMT modulation in breast cancer.

Enhancement of immunogenicity of murine lymphocytic leukemia cells by transfection with BCG heat shock protein 70 gene.

The effects of BCG heat shock protein 70 (BCG HSP70) gene transfection on tumorigenicity and immunogenicity of murine lymphocytic leukemia cell line (L1210) were studied. After HSP70 gene transfection, the tumor cells became strongly immunogenic and lost their tumorigenicity in syngeneic mice. It mainly exhibited that tumor growth was slow or without the formation of tumor, mean survival time of mice was significantly prolonged and a marked stimulating effect on L1210 specific Th1 cells detected by IFN-γ ELISPOT assay. Tumor-bearing mice treated with the L1210-HSP70 cells showed thorough coagulation necrosis and abundant CD8+ T lymphocyte infiltration. Meanwhile, as the tumor vaccine, the HSP70-transfected tumor cells could induce a protective immune response in vivo. It showed that the tumor growth was significantly inhibited, tumor diameter was markedly reduced and the survival time of tumor-bearing mice was further prolonged. Immunization with it also resulted in regression of the established L1210 tumor and prolonged survival time of mice. These results suggest that gene transfection of BCG HSP70 could effectively improve the immunogenicity of tumor cells and it may be used as a suitable candidate gene-modified cell vaccine for cancer immunotherapy.

[The progressive effects of chronic intermittent hypoxia on cognitive function and the cholinergic neuron in rats].

OBJECTIVE: To investigate the relation between the progressive effects of chronic intermittent hypoxia (CIH) on cognitive function and the change of cholinergic neuron. METHODS: Forty adult male Sprague-Dawley rats were randomly averagely divided into four groups: control group, CIH 1 week group, CIH 3 week group and CIH 5 week group. The cognitive function was assessed by the Morris Water Maze. The necrosis neurons in prefrontal cortex and hippocampus were observed and counted. The cholin acetyltransferase (ChAT) immunostained cells in prefrontal cortex and hippocampus were identified and quantitated. RESULTS: The spatial learning and memory impairments progressed from 1 to 5 5 weeks in rats. Compared with the control group, the cognitive impairments in CIH5w group were significant (P < 0.05). The degeneration or necrosis neurons in prefrontal cortex and hippocampus were significantly increased in CIH rats, and worsen gradually along with the hypoxia. The ChAT immunostained cells in prefrontal cortex and hippocampus were gradually reduced. The ChAT immunostained cells of prefrontal cortex and hippocampus in CIH3w group and CIH5w group were less than that in control group (P < 0.05). CONCLUSION: Chronic intermittent hypoxia induced slowly progressive spatial learning and memory impairments in rats, which maybe associated with the damage of neurons and the reduction of ChAT in prefrontal cortex and hippocampus.

[ZNF185 gene cloning and the localization in mouse testis].

AIM: we Clone the ZNF185 gene and detect the position of ZNF185 in the mouse testis. METHODS: extracted from mouse testis RNA, by RT-PCR, and then the obtained fragment was cloned and identified; extracted from mouse liver, testis and ovary proteins were Western blot analysis; preparation of frozen sections of mouse testes, immunofluorescence techniques analysis. RESULTS: (1) ZNF185 gene cloning was correct. (2) Western blot showed that the most abundant in the testes ZNF185. (3) Immunofluorescence showed, ZNF185 located in Leydig cells and sperm, Leydig cells in the weak, and in round spermatids and mature sperm were highly expressed. CONCLUSION: the gene cloning of ZNF185 was successful and initially proved the position of ZNF185 in the mouse testis.