LncRNA-MALAT1 as a novel biomarker of cadmium toxicity regulates cell proliferation and apoptosis.

Cadmium (Cd) and its compounds are well-known human carcinogens, but the mechanisms underlying the carcinogenesis are not well understood. This study aimed to investigate whether lncRNA-MALAT1 could serve as a novel biomarker of Cd toxicity in cells, animals and Cd-exposed workers, and regulate cell proliferation, apoptosis, migration and invasion. MALAT1 expression increased gradually in CdCl transformed 16HBE cells.

regulates migration, invasion and apoptosis in cadmium transformed 16HBE cells and is a novel biomarker of cadmium exposure in a rat model and in workers.

Translation (eukaryotic) initiation factor 3 ( or ) has been found to be a proto-oncogene in cadmium (Cd) response both and , but whether may serve as a biomarker of Cd exposure is still unclear. This study aimed to investigate whether could serve as a novel biomarker of Cd toxicity in cells, animals and workers, and regulate the apoptosis, migration and invasion in human bronchial epithelial cell (16HBE cells) transformation with cadmium chloride (CdCl). In CdCl transformed 16HBE cells, expression increased gradually, and sequencing did not identify mutation and methylation of .

Long non-coding RNAs as novel expression signatures modulate DNA damage and repair in cadmium toxicology.

Increasing evidence suggests that long non-coding RNAs (lncRNAs) are involved in a variety of physiological and pathophysiological processes. Our study was to investigate whether lncRNAs as novel expression signatures are able to modulate DNA damage and repair in cadmium(Cd) toxicity. There were aberrant expression profiles of lncRNAs in 35th Cd-induced cells as compared to untreated 16HBE cells.

[Intracranial atherosclerotic middle cerebral arterial stenosis research based on 3.0 Tesla high-resolution magnetic resonance imaging: recent progress].

Intracranial atherosclerotic disease (ICAD) of a major intracranial artery, including middle cerebral artery (MCA),basilar artery, is the most common causes of stroke and is associated with a high risk of recurrent stroke in China. The difficulty to treatment these high-risk disease is to identify high-risk stroke subgroups and to develop more effective treatments (aggressive medical therapy/endovascular therapy). With the benefits, including non-invasive, in vivo, and no-ionizing radiation, 3.

Cadmium induced cell apoptosis, DNA damage, decreased DNA repair capacity, and genomic instability during malignant transformation of human bronchial epithelial cells.

Cadmium and its compounds are well-known human carcinogens, but the mechanisms underlying the carcinogenesis are not entirely understood. Our study was designed to elucidate the mechanisms of DNA damage in cadmium-induced malignant transformation of human bronchial epithelial cells. We analyzed cell cycle, apoptosis, DNA damage, gene expression, genomic instability, and the sequence of exons in DNA repair genes in several kinds of cells.