Signal Transducer and Activator of Transcription 4-Induced Up-Regulated LINC01278 Enhances Proliferation and Invasion of Non-Small Cell Lung Cancer Cells via the MicroRNA-877-5p/Activating Transcription Factor 4 Axis.

Background: The purpose of this study was to investigate the specific effects of signal transducer and activator of transcription 4 (STAT4)-induced long intergenic nonprotein coding RNA 1278 (LINC01278) on the growth of non-small cell lung cancer (NSCLC) cells involved in the microRNA (miR)-877-5p/activated transcription factor 4 (ATF4) axis.

Methods: NSCLC tumor tissue and adjacent normal tissue were collected. Human normal lung epithelial cell BEAS-2B and human NSCLC cell lines (H1299, H1975, A549, H2228) were collected.

The Akt pathway mediates the protective effects of myeloid differentiation protein 1 in pathological cardiac remodelling.

Aims: Myeloid differentiation protein 1 (MD1) was shown to ameliorate pressure overload-induced cardiac hypertrophy and fibrosis by negatively regulating the MEK-ERK1/2 and NF-κB pathways. However, whether MD1 modulates cardiac function and whether the Akt pathway mediates the benefits of MD1 in pressure overload-induced cardiac remodelling remain unclear.

Methods And Results: Male cardiac-specific transgenic MD1 (MD1-TG) mice, MD1-knockout (KO) mice and wild-type (WT) littermates aged 8-10 weeks were subjected to sham operation and aortic banding (AB) for 4 weeks.

Sevoflurane inhibits cell proliferation and migration of glioma by targeting the miR‑27b/VEGF axis.

Poor prognosis in patients with glioma is primarily due to rapid tumor growth and cell invasion and migration. In addition, microRNA (miR)‑27b is decreased in metastatic glioma. The present study investigated whether sevoflurane inhibited glioma cell progression by targeting miR‑27b.

Cyanidin‑3‑O‑β‑glucoside protects against pulmonary artery hypertension induced by monocrotaline via the TGF‑β1/p38 MAPK/CREB signaling pathway.

Pulmonary artery hypertension (PAH) is a disease with high morbidity and mortality. Cyanidin‑3‑O‑β‑glucoside (Cy‑3‑g), a classical anthocyanin, has a variety of biological effects. The present study evaluated whether Cy‑3‑g attenuated PAH, and explored the potential mechanism of action.

Ciliary neurotrophic factor overexpression protects the heart against pathological remodelling in angiotensin II-infused mice.

Background: Ciliary neurotrophic factor (CNTF), which is a neural peptide, has been reported to confer cardioprotective effects. However, whether CNTF-based gene therapy could prevent cardiac remodelling remains incompletely clear. In this study, we used adeno-associated viral vector serotype 9 (AAV9)-based cardiac gene therapy to test the effects of CNTF overexpression on adverse ventricular remodelling in angiotensin II (Ang II)-infused mice.

CircRNA circ_0004370 promotes cell proliferation, migration, and invasion and inhibits cell apoptosis of esophageal cancer via miR-1301-3p/COL1A1 axis.

Background: The aim of this study was to investigate the circ_0004370 expression in EC, its effects on cell proliferation, apoptosis, migration, invasion, and epithelial-mesenchymal transition (EMT) process, and the underlying regulatory mechanisms in EC.

Methods: The protein levels of COL1A1 and EMT-related proteins were detected by western blot. The role of circ_0004370 on cell viability, proliferation, and apoptosis was analyzed by Cell Counting Kit-8 (CCK-8) assay, colony formation assay, and flow cytometry, respectively.

MicroRNA-34c-3p target inhibiting NOTCH1 suppresses chemosensitivity and metastasis of non-small cell lung cancer.

Background: Chemotherapy is the standard treatment for non-small cell lung cancer (NSCLC). However, chemoresistance frequently occurs, making the treatment of NSCLC more difficult.

Method: We combined clinical and experimental studies to establish the role of microRNA (miR)-34c in NSCLC metastasis and chemoresistance.

Aquaporin-2 expression in the kidney and urine is elevated in rats with monocrotaline-induced pulmonary heart disease.

Objective: Little is known about how renal aquaporin-2 (AQP2) expression is affected by right heart failure caused by pulmonary heart disease (PHD). Therefore, we examined the expression of AQP2 in a rat model of PHD induced by monocrotaline (MCT).

Methods: After 4 weeks of treatment, urine and blood samples were collected from sham-treated and MCT-treated rats.

MicroRNA-183-3p up-regulated by vagus nerve stimulation mitigates chronic systolic heart failure via the reduction of BNIP3L-mediated autophagy.

Chronic systolic heart failure (CSHF) was a complex syndrome. Recently, vagus nerve stimulation (VNS), a novel treatment method, has emerged for the treatment of CSHF. therefore the aim of this study was to explore the possible mechanism of VNS treatment alleviating CSHF in rats.