Notes

Smart Warning Engineering for IoT.
This analysis process was effective to construct ceRNA network. The result will be conductive to explore the significant lncRNAs and regulatory mechanism.
The identified lncRNAs were promising candidate biomarkers in HCC diagnosis and therapeutics. This analysis process was effective to construct ceRNA network. The result will be conductive to explore the significant lncRNAs and regulatory mechanism.
Long noncoding RNA (lncRNA) is emerging as a vital regulator in various tumors. However, the biological function of ZFPM2-antisense RNA 1 (ZFPM2-AS1) in hepatocellular carcinoma (HCC) remains unclear. The present study aims to explore the function and mechanism of ZFPM2-AS1 in hepatocellular carcinoma progression.

The ZFPM2-AS1 expression in HCC cells and tissues was measured by quantitative real-time polymerase chain reaction (qRT-PCR). Effects of ZFPM2-AS1 on tumor cell proliferation and invasion were detected by CCK8 assay or EdU assay or matrigel migration assay and Western blot. The Luciferase reporter assay, RNA pulldown assay, qRT-PCR, and Western blot were performed to explore and confirm the interaction between ZFPM2-AS1 and miR-1226-3p and integrin β1 (ITGB1).

ZFPM2-AS1 was overexpressed in HCC tissues and cell lines. High levels of ZFPM2-AS1 were correlated with advanced TNM stage, distant metastasis and a poorer overall survival rate. ZFPM2-AS1 knockdown inhibited cell proliferation and invasion. ZFPM2-AS1 could directly bind to and negatively regulate miR-1226-3p expression. Moreover, ITGB1 was identified as a target gene of miR-1226-3p. ITGB1 was found to be directly negatively regulated by miR-1226-3p and indirectly upregulated by ZFPM2-AS1. Rescue assays demonstrated that ZFPM2-AS1 promotes HCC cell proliferation and invasion through modulating miR-1226/ITGB1 axis.

ZFPM2-AS1 promotes cell proliferation and migration by regulating miR-1226-3p/ITGB1 axis in HCC.
ZFPM2-AS1 promotes cell proliferation and migration by regulating miR-1226-3p/ITGB1 axis in HCC.
Long-chain non-coding RNA (LncRNA) is abnormally expressed in various malignant tumors. In recent years, it has been found that the expression of LncRNA SNHG6 is upregulated in gallbladder carcinoma tissues, which participated in the occurrence and development of gallbladder carcinoma. However, the clinical value of SNHG6 in gallbladder cancer serum is not clear, and there are few studies regulating the biological function of gallbladder carcinoma cells. This study aimed to investigate LncRNA SNHG6 and miR-26b-5p in gallbladder carcinoma and its related mechanisms.

From February 2017 to February 2019, altogether 68 cases of gallbladder cancer patients admitted to the Yantai Yeda Hospital were collected as a study group, 70 healthy people as a control group. Gallbladder cancer cells and human colorectal mucosa cells were purchased. Sh-SNHG6, si-SNHG6, NC, miR-26b-5p-inhibitor, and miR-26b-5p-mimics were transfected into GBC-SD and NOZ cells. For the detection of SNHG6 and miR-26b-5p in samples we used qRT- targeted relationship. Rescue experiments showed that after co-transfecting sh-SNHG6+miR-26b-5p-mimics, and si-SNHG6+miR-26b-5p-inhibitor into GBC-SD and NOZ, the proliferation, invasion and apoptosis of cells were not different from those of miR-NC group without transfection sequence.

Inhibition of LncRNA SNHG6 expression can upregulate miR-26b-5p mediated Hedgehog signaling pathway, affect epithelial-mesenchymal transition, proliferation and invasion of cells, so LncRNA SNHG6is hoped to be a latent therapeutic target for gallbladder carcinoma.
Inhibition of LncRNA SNHG6 expression can upregulate miR-26b-5p mediated Hedgehog signaling pathway, affect epithelial-mesenchymal transition, proliferation and invasion of cells, so LncRNA SNHG6is hoped to be a latent therapeutic target for gallbladder carcinoma.
This review aimed at examining efficacy of interventional radiotherapy (brachytherapy-IRT) alone or combined with external beam radiotherapy (EBRT) in stage I esophageal cancer as exclusive treatment.

A systematic research using PubMed, Scopus, and Cochrane library was performed. ClinicalTrials.gov was searched for ongoing or recently completed trials, and PROSPERO was searched for ongoing or recently completed systematic reviews. We analyzed only clinical study as full-text publication, reporting on patients with stage I esophageal cancer treated with IRT alone or in combination with other treatments (e.g., EBRT). Conference paper, survey, letter, editorial, book chapter, and review were excluded. HDAC inhibitor Patients who underwent previous surgery were excluded. Time restriction (1990-2018) was applied for years of the publication.

Twelve studies have been selected. The number of evaluated patients was 514; the median age was 69 years. In the IRT group, the median local control (LC) was 77% (range 63%-100%), disease-free survival (DFS) was 68.4% (range 49%-86.3%), the overall survival (OS) was 60% (range 31%-84%), the cancer specific survival (CSS) was 80% (range 55-100%), and grade 3-4 toxicity range was 0%-26%.

IRT alone or combined to EBRT is an effective and safe treatment option for patients with stage I esophageal cancer. Definitive radiation therapy could be an alternative to surgery in patients with superficial cancer.
IRT alone or combined to EBRT is an effective and safe treatment option for patients with stage I esophageal cancer. Definitive radiation therapy could be an alternative to surgery in patients with superficial cancer.
We aimed to explore the expression of circRNA_009934 in osteoclast, as well as its potential roles in regulating osteoclastogenesis and bone resorption via regulating miR-5107.

We performed qRT-PCR analysis to examine the expression of circRNA_009934 in osteoclast in distinctive stages. We used CCK-8 assay to detect the cell proliferation ability. Correlation analysis between the expression levels of circRNA_009934 and miR-5107 was performed using statistical analysis. Bioinformatics prediction was performed to predict the binding site of circRNA_009934 and miR-5107, subsequently followed by Luciferase assay for validation. The mice TRAF6 3'-UTR were cloned into the Luciferase reporter vector and miR-5107 binding mutants were constructed to validate the inhibited regulation of miR-5107 to the expression of TRAF6.

Our results showed that expression of circRNA_009934 was increased during osteoclast differentiation. CircRNA_009934 expression was closely correlated with osteoclastogenesis and bone resorption activity.
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