Exosomal HSPB1, interacting with FUS protein, suppresses hypoxia-induced ferroptosis in pancreatic cancer by stabilizing Nrf2 mRNA and repressing P450.

Ferroptosis is a new type of programmed cell death, which has been involved in the progression of tumours. However, the regulatory network of ferroptosis in pancreatic cancer is still largely unknown. Here, using datasets from GEO and TCGA, we screened HSPB1, related to the P450 monooxygenase signalling, a fuel of ferroptosis, to be a candidate gene for regulating pancreatic cancer cell ferroptosis.

Myoglobin improves doxycycline sensitivity in pancreatic cancer through promoting heme oxygenase-1-mediated ferroptosis.

Ferroptosis is expected to be a therapeutic target for cancers including pancreatic cancer. We aimed to screen genes that regulate ferroptosis and doxycycline resistance in pancreatic cancer and to explore the underlying mechanisms. Bioinformatics analysis was performed to identify genes that respond to ferroptosis in two human pancreatic cancer cells with GOT1 knocked down or not.

Effect of fluvalinate on the expression profile of circular RNA in brain tissue of workers.

Fluvalinate is widely used in apiculture as an acaricide for removing Varroa mites, but there have been growing concerns about the negative effects of fluvalinate on honeybees in recent years. Previous research revealed changes in the miRNA and mRNA expression profiles of brain tissues during fluvalinate exposure, as well as key genes and pathways. The role of circRNAs in this process, however, is unknown.

Transcriptomic analysis to elucidate the response of ligustica brain tissue to fluvalinate exposure.

As a commonly used acaricide in apiculture, fluvalinate is used to kill Varroa mites, while it also damages the nervous system of honeybees. To date, the transcriptomic characteristics associated with fluvalinate-induced neuronal injury in the bee brain have not been reported. Here, we performed transcriptome sequencing on ligustica ( ligustica) brain tissues collected before and after fluvalinate treatment.

[Expression of HMGB-1 and its extracellular release of cultured primary hepatic parenchymal cells and Kupffer cells induced by LPS].

Objective: To investigate HMGB-1 expression and its extracellular release of cultured primary hepatic parenchymal cells (HC) and Kupffer cells (KC) that were induced by lipopolysaccharides (LPS).

Methods: Primary hepatic parenchymal cells and Kupffer cells were cultured in flasks, and some cells were treated with 500 microg/L LPS for 24 hours (induced group) and some were not treated with LPS and served as controls. All of the cells were repeatedly frozen-thawed, and the expression levels of HMGB1-mRNA and HMGB1 proteins were detected by semi-quantitative RT-PCR and Western blot respectively.