MiR-202-3p Targets Calm1 and Suppresses Inflammation in a Mouse Model of Acute Respiratory Distress Syndrome.

Acute respiratory distress syndrome (ARDS) is regarded as a type of respiratory failure. Emerging evidence has demonstrated the significant roles of microRNAs in various disorders. Nevertheless, the role of miR-202-3p in ARDS is unclear.

BRD7 restrains TNF-α-induced proliferation and migration of airway smooth muscle cells by inhibiting notch signaling.

: Bromodomain-containing protein 7 (BRD7) is a key component of the switch/sucrose non-fermentable complex that participates in chromatin remodeling and transcriptional regulation. Although the emerging role of BRD7 in the pathophysiology of various diseases has been observed, its role in asthma remains unknown. Here, we assessed the function of BRD7 as a mediator of airway remodeling in asthma using an model.

An SETD1A/Wnt/β-catenin feedback loop promotes NSCLC development.

Background: SETD1A, a member of SET1/MLL family H3K4 methyltransferases, is involved in the tumorigenesis of numerous cancers. However, the biological role and mechanism of SETD1A in non-small cell lung cancer (NSCLC) remain to be elucidated.

Methods: The expression of SETD1A, NEAT1, EZH2, and β-catenin in NSCLC tissues and cell lines was detected by qRT-PCR, immunohistochemistry and western blotting.

The interplay between ATF2 and NEAT1 contributes to lung adenocarcinoma progression.

Background: Activating transcription factor 2 (ATF2), a member of the activator protein 1 (AP-1) transcription factor family, has been shown to be involved in the pathobiology of numerous cancers. However, the biological role and mechanism of ATF2 in lung adenocarcinoma (LUAD) remains to be elucidated.

Methods: The expression of ATF2, NEAT1 and miR-26a-5p in LUAD tissues and cell lines was detected by qRT-PCR and western blotting.

Increased chemokines levels in patients with chronic obstructive pulmonary disease: correlation with quantitative computed tomography metrics.

Objective: We sought to explore the relationships between multiple chemokines with spirometry, inflammatory mediators and CT findings of emphysema, small airways disease and bronchial wall thickness.

Methods: All patients with COPD ( = 65) and healthy control subjects ( = 23) underwent high-resolution CT, with image analysis determining the low attenuation area (LAA), ratio of mean lung attenuation on expiratory and inspiratory scans (E/I MLD) and bronchial wall thickness of inner perimeter of a 10-mm diameter airway (Pi10). At enrollment, subjects underwent pulmonary function studies, chemokines and inflammatory mediators measurements.

MicroRNA-147b suppresses the proliferation and invasion of non-small-cell lung cancer cells through downregulation of Wnt/β-catenin signalling via targeting of RPS15A.

Deregulation of microRNAs (miRNAs) leads to malignant growth and aggressive invasion during cancer occurrence and progression. miR-147b has emerged as one of the cancer-related miRNAs that are dysregulated in multiple cancers. Yet, the relevance of miR-147b in non-small-cell lung cancer (NSCLC) remains unclear.

NEAT1/miR‑124/STAT3 feedback loop promotes breast cancer progression.

The long non‑coding RNA nuclear enriched abundant transcript 1 (NEAT1) has important roles in the regulation of multiple cell functions, such as proliferation, apoptosis and migration. However, the mechanism by which NEAT1 regulates breast cancer progression is not well elucidated. In the present study, NEAT1 and microRNA‑124 (miR‑124) levels were detected by reverse transcription‑quantitative PCR in breast cancer tissues and cell lines.

miR-145-5p is associated with smoke-related chronic obstructive pulmonary disease via targeting KLF5.

Increasing evidence illustrate that dysregulation of microRNAs (miRNAs) is involved in the pathogenesis of chronic obstructive pulmonary disease (COPD), which is mainly resulted from cigarette smoke (CS) exposure. However, the role of miR-145-5p in CS-mediated COPD remains largely unknown. Thus, the aim of this study was to investigate the expression level of miR-145-5p in 31 human lung tissues samples, and to explore its regulatory role in the apoptosis and inflammation of human bronchial epithelial cells (HBECs) following CS extract (CSE) exposure.

MYC and DNMT3A-mediated DNA methylation represses microRNA-200b in triple negative breast cancer.

Triple-negative breast cancer (TNBC) is the most aggressive breast cancer subtype with a poor prognosis. The microRNA-200 (miR-200) family has been associated with breast cancer metastasis. However, the epigenetic mechanisms underlying miR-200b repression in TNBC are not fully elucidated.

A miR-26a/E2F7 feedback loop contributes to tamoxifen resistance in ER-positive breast cancer.

Tamoxifen (TAM) resistance is a substantial challenge in the treatment of estrogen receptor (ER)-positive breast cancer. Previous studies have revealed an important role of microRNA (miRNA/miR)-26a in TAM resistance in breast cancer. However, the mechanism underlying the regulatory effects of miR-26a on TAM resistance remains to be elucidated.

Nano Let‑7b sensitization of eliminating esophageal cancer stem‑like cells is dependent on blockade of Wnt activation of symmetric division.

The poor therapy response and poor prognosis of esophageal cancer has made it one of the most malignant carcinoma, and the complicated multidisciplinary treatment failed to achieve a long-term disease-free survival. To diagnose esophageal cancer at an earlier stage, and to improve the effect of anticancer therapy would improve the therapeutic efficacy. After retrospective analysis of the cancer samples of patients who received esophagectomy, we found the relevance between ratio of either ALDH1 or CD133-positive cancer stem cells and 2-year recurrence.

Emodin suppresses silica-induced lung fibrosis by promoting Sirt1 signaling via direct contact.

Pulmonary silicosis is characterized by lung fibrosis, which leads to impairment of pulmonary function; the specific mechanism remains to be fully elucidated Emodin shows antifibrotic effects in several organs with fibrosis, however, it has not been investigated in pulmonary silicosis. In the present study, the possible mechanism of lung fibrosis and the antifibrotic effect of emodin in silica inhalation‑induced lung fibrosis were investigated. Pulmonary silica particle inhalation was used to induce lung fibrosis in mice.

CDH1 promoter methylation correlates with decreased gene expression and poor prognosis in patients with breast cancer.

The E-cadherin gene (CDH1) is associated with poor prognosis and metastasis in patients with breast cancer, and methylation of its promoter is correlated with decreased gene expression. However, there is currently no direct evidence that CDH1 promoter methylation indicates poor prognosis in patients with breast cancer. In the present study, methylation-specific polymerase chain reaction (PCR) was applied to detect the methylation status of the CDH1 promoter in 137 primary breast cancer, 85 matched normal breast tissue and 13 lung metastasis specimens.

[miR-101 inhibits the proliferation and migration of breast cancer cells via downregulating the expression of DNA methyltransferase 3a].

Objective: To investigate the effect of microRNA-101 (miR-101) on the proliferation and migration of breast cancer cells and its possible mechanism.

Methods: The expressions of miR-101 and DNA methyltransferase 3a (DNMT3a) in breast cancer tissues, corresponding normal breast tissues, breast cancer cells and normal breast cells were detected by real-time quantitative PCR. The lentiviral vectors containing miR-101 and shRNA-DNMT3a sequences were transfected into MDA-MB-231 cells to regulate the expressions of miR-101 and DNMT3a.