LncRNA TUG1 promotes esophageal cancer development through regulating PLK1 expression by sponging miR-1294.

Objectives: Esophageal cancer is one of the malignant tumor with poor survival. The 5-year survival rate of esophageal cancer patients remains poor due to limited therapeutic options and the development of drug-resistance. Recent evidence suggests that long non-coding RNAs (lncRNAs) are involved in occurrence and development of tumor, however, the molecular mechanisms of lncRNA taurine-upregulated gene 1 (TUG1) in esophageal cancer remain unknown.

pH/redox sequentially responsive nanoparticles with size shrinkage properties achieve deep tumor penetration and reversal of multidrug resistance.

Multidrug resistance (MDR) remains a serious impediment to successful tumor chemotherapy. Despite considerable efforts to address MDR, limited approaches have been successful in the clinic to date. Here, we have developed pH/redox cascade-sensitive multiscale nanoparticles (DMA-NPs) with size- and charge-changeable properties for the efficient delivery of a non-P-glycoprotein substrate anticancer drug (podophyllotoxin, PPT) to combat MDR.

miR-203 affects esophageal cancer cell proliferation, apoptosis and invasion by targeting MAP3K1.

miR-203 has been indicated to be a tumor suppressor in esophageal cancer, however, the underlying molecular mechanisms by which it functions are not fully understood. The present study aimed to investigate the molecular mechanisms underlying the regulatory activities of microRNA (miR)-203 in esophageal cancer. The miR-203 mimic/inhibitor, Mitogen-Activated Protein Kinase Kinase Kinase 1 (MAP3K1) overexpression plasmid and MAP3K1 small interfering (si)RNA were transfected into TE-1 cells.

S1PR1 promotes proliferation and inhibits apoptosis of esophageal squamous cell carcinoma through activating STAT3 pathway.

Background: Esophageal squamous cell carcinoma (ESCC) is one of the most common cancers worldwide, which lacks effective biomarkers for prognosis. Therefore, it is urgent to explore new potential molecular markers to discriminate patients with poorer survival in ESCC.

Methods: Bioinformatics analysis, qRT-PCR, and western blot were applied to investigate S1PR1 expression.

The effects of miR-429 on cell migration and invasion by targeting Slug in esophageal squamous cell carcinoma.

Increasing evidence indicates that microRNAs may play important roles in tumor development and may take part in different processes in different cancers. miR-429 is known as a cancer suppressor or oncogene that is dysregulated in different malignancies, including esophageal squamous cell carcinoma (ESCC). However, the effect of miR-429 in ESCC has not been fully explored.

Removal of chromium (VI) from water using nanoscale zerovalent iron particles supported on herb-residue biochar.

A composite material consisting of nanoscale zerovalent iron particles supported on herb-residue biochar (nZVI/BC) was synthesized and used for treatment of Cr(VI)-contaminated water. The effects of initial pH, chromium concentration, contact time, and competition with coexisting anions and natural organic matter (NOM) were also investigated. nZVI/BC was characterized by X-ray diffraction (XRD), transmission electron microscopy (TEM), and scanning electron microscopy analysis (SEM), and the Brunauer-Emmett-Teller surface area was measured.

Poly(C)-binding protein 1 mediates drug resistance in colorectal cancer.

Oxaliplatin (L-OHP) is standard treatment for colorectal cancer. However, resistance to L-OHP often leads to treatment failure or cancer relapse. Understanding of the mechanism underlying L-OHP resistance is important to overcome the resistance and improve colorectal cancer treatment.

[Effect of homoharringtonine on expression of NF-κB and BCL-2 proteins in K562 cells].

This study was aimed to investigate the effect of homoharringtonine (HHT) on K562 cell proliferation, apoptosis and expression of BCL-2 and NF-κB proteins. The cells proliferation was assayed with MTT method, the cell apoptosis, cell cycle and BCL-2 expression were analyzed with flow cytometry, NF-κB protein expression was detected with Western blot. The results showed that HHT concentration-dependently inhibited proliferation of K562 cells, the IC50 at 48 h was 43.