CYP3A4 gene expression discloses individual differences in postoperative pain susceptibility and drug treatment response in patients with lung cancer.

This study investigates the influence of CYP3A4 gene polymorphisms on postoperative pain sensitivity and analgesic response in lung cancer patients undergoing intercostal nerve block with local anesthetics. Sixty patients (ages 31-74) undergoing thoracoscopic lung cancer surgery were enrolled and divided into two groups based on CYP3A4 gene expression level: Group I (high CYP3A4) and Group II (low CYP3A4). Postoperative pain was assessed using the Visual Analogue Scale (VAS), and patient-controlled intravenous analgesia (PCIA) pump usage, ECG ST-T segment changes, complications, hospital stay, and costs were recorded.

Circular RNA La-related protein 4 inhibits cell proliferation, migration, and invasion and sponges microRNA-367 in non-small cell lung cancer.

This study aimed to investigate the effect of circular RNA (circRNA) La-related protein 4 (LARP4) on inhibiting the malignant progression of non-small cell lung cancer (NSCLC) cells. CircRNA LARP4 expression in a human normal lung epithelial cell line and NSCLC cell lines was detected by reverse transcription-quantitative polymerase chain reaction. CircRNA LARP4 overexpression and control overexpression plasmids were transfected into NCI-H1650 cells; circRNA LARP4 knockdown and control knockdown plasmids were transfected into A549 cells.

Arsenic trioxide inhibits Skp2 expression to increase chemosensitivity to gemcitabine in pancreatic cancer cells.

The S-phase kinase associated protein 2 (Skp2), a member of the F-box protein family, regulates cell cycle progression and is highly expressed in pancreatic cancer (PC). Recently, we reported that arsenic trioxide (ATO) inhibited cell growth and invasion via downregulation of Skp2 in PC cells. Emerging evidence has revealed that Skp2 plays a crucial role in drug resistance in several kinds of cancers.

Detection of c-kit mutational status in small-cell lung cancer in a Chinese cohort.

Background: Overexpression of KIT (CD117), a tyrosine kinase receptor, and its natural ligand, stem cell factor, are found in small-cell lung cancer (SCLC). Somatic mutations of the proto-oncogene c-kit constitutively activate KIT expression in a ligand-independent way. To explore the clinical value of the c-kit mutation as a potential target for therapy with tyrosine kinase inhibitors, the c-kit mutational status and KIT expression in tumors from Chinese patients with SCLC were analyzed.