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 CdCl2 transformed 16HBE cells. The cell apoptosis, migration and invasion were significantly inhibited, and the mRNA and protein expression of FOXC2, STAT, BAX, EGFR, and TGF-β1 reduced, but BCL-2 increased (P < 0.05) after silencing MALAT1 by siRNA in CdCl2 treated 16HBE cells of 15th and 35th passages. Cadmium increased MALAT1 expression in the lung of Cd-exposed rats in a dose-dependent manner. A significant positive correlation was observed between blood MALAT1 expression and urinary/blood Cd concentrations, and there were significant correlations of MALAT1 expression with the expressions of target genes in the lung of Cd-exposed rats and the blood of Cd exposed workers. This study suggests that the expression of MALAT1 is upregulated and regulates the cell cycle progression, proliferation, apoptosis, migration and invasion in Cd toxicity. MALAT1 may serve as a novel valuable biomarker of cadmium exposure and cadmium toxicity.

中文翻译：

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LncRNA-MALAT1作为镉毒性的新型生物标志物，可调节细胞增殖和凋亡。

镉（Cd）及其化合物是众所周知的人类致癌物，但致癌作用的机理尚不清楚。这项研究旨在调查lncRNA-MALAT1是否可以作为细胞，动物和镉暴露工人中镉毒性的新生物标记，并调节细胞增殖，凋亡，迁移和侵袭。在CdCl2转化的16HBE细胞中，MALAT1表达逐渐增加。CdCl2处理的siRNA沉默MALAT1后FOXC2，STAT，BAX，EGFR和TGF-β1的表达降低，细胞凋亡，迁移和侵袭受到抑制，mRNA和蛋白表达降低，但BCL-2升高（P <0.05）。第15和35代的16HBE细胞。镉以剂量依赖的方式增加了Cd暴露大鼠肺中MALAT1的表达。血液中MALAT1表达与尿/血Cd浓度之间存在显着的正相关，并且在暴露于Cd的大鼠的肺部和接触Cd的工人的血液中，MALAT1的表达与靶基因的表达之间存在显着的相关性。这项研究表明，MALAT1的表达上调并调节细胞周期进展，增殖，凋亡，迁移和Cd毒性侵袭。MALAT1可以作为镉暴露和镉毒性的新型有价值的生物标记。这项研究表明，MALAT1的表达上调并调节细胞周期进展，增殖，凋亡，迁移和Cd毒性侵袭。MALAT1可以作为镉暴露和镉毒性的新型有价值的生物标记。这项研究表明，MALAT1的表达上调并调节细胞周期进展，增殖，凋亡，迁移和Cd毒性侵袭。MALAT1可以作为镉暴露和镉毒性的新型有价值的生物标记。