Since humans and leatherbacks may experience prolonged exposure to Cr(VI), and prolonged Cr(VI) exposure leads to carcinogenesis in humans, in this study we considered both acute and prolonged exposures.
Through comprehensive review of available literature found between 1973 and 2019, this article provides a summary of updated understanding of the molecular mechanisms of Cr(VI)-carcinogenesis.
It was further determined that overexpressing miR-494 significantly reduces Cr(VI)-induced CSC-like property, cell transformation, and tumorigenesis mainly through down-regulating c-Myc expression.
Here, we discuss the impact of Cr(VI) on the stress response-an intricate cellular system against proteotoxic stress which is increasingly viewed as playing a critical role in carcinogenesis.
The present study demonstrated that upregulation of SIRT3 causes mitophagy suppression and plays an important role in cell survival and tumorigenesis of Cr(VI)-transformed cells.
Findings support the influence of epigenetic alterations on cell signaling related to Cr(VI)-induced cytotoxicity/cell proliferation, and decreases in DNA repair signaling leading to tumorigenesis.
These outcomes support the hypothesis that CIN is a key mechanism of Cr(VI)-induced carcinogenesis.<b>Significance:</b> Chromium, a major public health concern and human lung carcinogen, causes fundamental changes in chromosomes and DNA repair in human lung cells.<i></i>.
To examine the mechanism of hexavalent chromium [Cr(VI)]-induced carcinogenesis, a cross-sectional study in workers with or without exposure to Cr(VI) as well as in vitro administration of Cr(VI) in 16HBE cells was conducted.
Stable knockdown of miR-21 and overexpression of PDCD4 or catalase in BEAS-2B cells suppressed Cr(VI)-induced malignant transformation and tumorigenesis.
Using a culture of mouse splenic T cells as an in vitro model system, the present study assessed the effects of Cr(VI) on T cells, as the first step in our investigation of the mechanism underlying Cr(VI)-inhibited immunosurveillance and carcinogenesis.
In this study, we investigated the potential role of Gene 33 (ERRFI1, Mig6), a multifunctional adaptor protein, in Cr(VI)-mediated lung carcinogenesis.
Multiple mechanisms have been shown to contribute to Cr(VI) induced carcinogenesis, including DNA damage, genomic instability, and epigenetic modulation, however, the molecular mechanism and downstream genes mediating chromium's carcinogenicity remain to be elucidated.
In this study, we investigated the role of NADPH oxidase (NOX), one of the major sources of cellular ROS, in Cr(VI)-induced oxidative stress and carcinogenesis.
In order to gain further insight into Cr(VI)-induced carcinogenesis, we have established an adequate in vitro cellular model for the study of this process.To this end, BEAS-2B cells were used.
Together these results clearly demonstrate that Cr(VI) exposure can greatly enhance the mutagenicity and cytotoxicity of PAHs by inhibiting the cellular NER pathway, and this may constitute an important mechanism for Cr(VI)-induced human carcinogenesis.