Transcriptional analysis of Bemisia tabaci MEAM1 cryptic species under the selection pressure of neonicotinoids imidacloprid, acetamiprid and thiamethoxam.

BACKGROUND: Neonicotinoids are widely applied in the control of the destructive agricultural pest Bemisia tabaci, and resistance against these chemicals has become a common, severe problem in the control of whiteflies. To investigate the molecular mechanism underlying resistance against nenonicotinoids in whiteflies, RNA-seq technology was applied, and the variation in the transcriptomic profiles of susceptible whiteflies and whiteflies selected by imidacloprid, acetamiprid and thiamethoxam treatment was characterized. RESULTS: A total of 90.86 GB of clean sequence data were obtained from the 4 transcriptomes. Among the 16,069 assembled genes, 584, 110 and 147 genes were upregulated in the imidacloprid-selected strain (IMI), acetamiprid-selected strain (ACE), and thiamethoxam (THI)-selected strain, respectively, relative to the susceptible strain. Detoxification-related genes including P450s, cuticle protein genes, GSTs, UGTs and molecular chaperone HSP70s were overexpressed in the selected resistant strains, especially in the IMI strain. Five genes were downregulated in all three selected resistant strains, including 2 UDP-glucuronosyltransferase 2B18-like genes (LOC 109030370 and LOC 109032577). CONCLUSIONS: Ten generations of selection with the three neonicotinoids induced different resistance levels and gene expression profiles, mainly involving cuticle protein and P450 genes, in the three selected resistant whitefly strains. The results provide a reference for research on resistance and cross-resistance against neonicotinoids in B. tabaci.

The relationship between gastric cancer, its precancerous lesions and bile reflux: A retrospective study.

OBJECTIVE: To evaluate the relationship between gastric cancer (GC) and precancerous lesions and bile reflux. METHODS: Medical records of 30 465 participants who underwent gastroscopy between January and December 2018 in our center were reviewed. Their age, sex, time of endoscopy, endoscopic/histologic diagnosis and grade of bile reflux were recorded. The participants were further divided into the chronic gastritis group (n = 27 807), a precancerous lesion group (n = 1943) and a GC group (n = 715). The χ2 tests and hierarchical analyses were performed. RESULTS: Patients aged 18-27 years had a higher bile reflux rate than those aged 28-37 and 68-75 years (P < 0.001), while it did not differ between patients aged <50 years and those over 50 years (P = 0.639). It was lower in men than in women (P < 0.001). The bile reflux rate did not differ in terms of months, seasons and half of the year (all P > 0.05), but differed between morning and afternoon when they underwent the endoscopy (P = 0.000). There was an interrelationship between the severity of gastric mucosal disease and bile reflux grade (r = 0.171). After excluding the effects of sex, age and time of endoscopy on bile reflux, bile reflux rate in chronic gastritis and precancerous lesions was lower than in gastric cancer (P < 0.01). CONCLUSIONS: Bile reflux may be a risk factor for gastric cancer and precancerous lesions. A high grade of bile reflux may be associated with the progression of gastric mucosal diseases.

PEITC triggers multiple forms of cell death by GSH-iron-ROS regulation in K7M2 murine osteosarcoma cells.

Phenethyl isothiocyanate (PEITC) is an isothiocyanate that largely exists in cruciferous vegetables and exhibits chemopreventive and chemotherapeutic potential against various cancers. However, it is little known about the molecular mechanisms of its antitumor action against osteosarcoma, which is the second highest cause of cancer-related death in children and adolescents. In this study, we investigated the effects of PEITC on K7M2 murine osteosarcoma both in vitro and in vivo. We found that treatment with PEITC dose-dependently inhibited the viability of K7M2 murine osteosarcoma cells with an IC50 value of 33.49 µM at 24 h. PEITC (1, 15, 30 µM) dose-dependently inhibited the cell proliferation, caused G2/M cell cycle arrest, depleted glutathione (GSH), generated reactive oxygen species (ROS), altered iron metabolism, and triggered multiple forms of cell death, namely ferroptosis, apoptosis, and autophagy in K7M2 cells. We further revealed that PEITC treatment activated MAPK signaling pathway, and ROS generation was a major cause of PEITC-induced cell death. In a syngeneic orthotopic osteosarcoma mouse model, administration of PEITC (30, 60 mg/kg every day, ig, for 24 days) significantly inhibited the tumor growth, but higher dose of PEITC (90 mg/kg every day) compromised its anti-osteosarcoma effect. Histological examination showed that multiple cell death processes were initiated, iron metabolism was altered and MAPK signaling pathway was activated in the tumor tissues. In conclusion, we demonstrate that PEITC induces ferroptosis, autophagy, and apoptosis in K7M2 osteosarcoma cells by activating the ROS-related MAPK signaling pathway. PEITC has promising anti-osteosarcoma activity. This study sheds light on the redox signaling-based chemotherapeutics for cancers.