Lung cancer is the first leading cause of cancer‑related death in the United States. Non‑small cell lung cancer (NSCLC) is the most common type of lung cancer and is associated with a poor patient prognosis. Identification of promising molecular targets is required for the effective prevention and therapy of NSCLC. Epithelial‑specific ETS‑1 (ESE‑1) belongs to the superfamily of ETS transcription factors. The effect of ESE‑1 on tumorigenesis is controversial in several types of cancer while its role in lung cancer remains unknown. The present study was designed to investigate whether ESE‑1 expression affects tumorigenic activity using human NSCLC cells and a mouse xenograft model. ESE‑1 expression suppressed anchorage‑independent growth in soft agar assay and led to an increase in G1 arrest and apoptosis in human NSCLC cells. ESE‑1 expression suppressed the invasion and migration of human NSCLC cells. Western blot analysis, RT‑PCR and promoter assay indicated that ESE‑1 expression was transcriptionally downregulated by treatment of transforming growth factor (TGF)‑β, an EMT (epithelial‑mesenchymal transition) stimulator. The xenograft study indicated that ESE‑1 expression inhibited tumor formation and development. Our data demonstrated that ESE‑1 plays a key role as a tumor suppressor in human NSCLC.

The soluble free, soluble conjugated, and insoluble bound phenolic compounds in tomato seeds were extracted and analyzed using ultra-high-performance liquid chromatography−high-resolution mass spectrometry. Total phenolic content (TPC) and free radical scavenging activities along with the antiproliferative effects against the human colorectal cancer cell line (HCT-116) were also examined for the soluble free, soluble conjugated, and insoluble bound phenolic fractions. 13, 7, and 10 compounds were tentatively identified in the soluble free, soluble conjugated, and insoluble bound phenolic fractions, respectively, including indole-3acetic acid derivatives, flavonoids, phenolic acid, and tyramine-derived hydroxycinnamic acid amines. The insoluble bound phenolic fraction was observed to have a greater TPC value and stronger free radical scavenging activities against ABTS •+ , DPPH • , and peroxyl radicals and a stronger inhibitory effect against HCT-116 cells compared with the soluble free and the soluble conjugated fractions. Soluble free and insoluble bound fractions significantly inhibited the proliferation of the HCT-116 cell line, and no antiproliferative effects were observed with the soluble conjugated fraction under the experimental conditions. The results may provide a foundation for future application of tomato seeds as nutraceuticals in dietary supplements and functional foods.

Oxidative stress is a main cause of tissue damage and highly associated with incidence of human chronic diseases. Among the major target organs attacked by reactive oxygen species (ROS) is the liver. Protocatechuic acid (PCA) is a phenolic compound found in green tea, acai oil and some mushroom species that possesses strong antioxidative and anti-inflammatory activity and may have benefits as a natural phytochemical for prevention of human diseases. However, the protective effect of PCA on hydrogen peroxide (H 2 O 2 )-induced oxidative stress specifically in the liver has not yet been investigated. The current study aims to observe if PCA possesses protective activity against H 2 O 2 -induced oxidative stress in HepG2 human liver cancer cells. Relative to untreated control cells, treatment of HepG2 cells with PCA reduced H 2 O 2 -induced cell death and mitigated H 2 O 2 -induced production of ROS; furthermore, it mitigated the H 2 O 2 -induced increase of caspase-3/7 enzyme activity, expression of cleaved poly(ADP-ribose) polymerase (PARP), expression of endoplasmic reticulum (ER) stress genes including activating transcription factor 4 (ATF4), serine/threonine-protein kinase/endoribonuclease inositol-requiring enzyme 1 α (IRE1α) and phosphorylation of p38 mitogen-activated protein kinases (MAPK). These findings indicate that PCA effectively protects hepatic cells from H 2 O 2 -induced oxidative stress and cell death.

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BACKGROUND Exposure to environmental chemicals has been linked with endothelial dysfunction, which is a leading cause of human diseases, including atherosclerosis. Permethrin is a frequently used synthetic pyrethroid insecticide for which longer exposure may cause toxicity in several types of tissues and the development of metabolic diseases, including atherosclerosis, obesity and diabetes. The present study was designed to evaluate the potential adverse effect of permethrin on the function and activity of human endothelial cells. RESULTS Permethrin was found to repress migration and tube formation by human umbilical vein endothelial cells (HUVECs) in a dose‐dependent manner, as well as to significantly repress their viability after 24 and 48 h of treatment. Furthermore, increased reactive oxygen species (ROS) production was observed in cells treated with permethrin, and the permethrin‐induced repression of cell viability was ROS‐dependent. Permethrin did not influence apoptosis, necrosis or mitochondrial membrane potential in HUVECs. CONCLUSION The results of the present study suggest that permethrin represses angiogenesis and viability through ROS‐dependent and cell growth‐, apoptosis‐ and necrosis‐independent means. © 2022 Society of Chemical Industry.