capable reduce carcinogenic cell invasiveness in carcinogenic cell

capable of causing or
exacerbating lung diseases by directly affecting signaling pathways involved in
cell migration, and remodeling of the airway. Therefore arsenic ingestion may
alter wound response and specifically, MMP-9/TIMP-1 ratios in the lung.

Following scrapewounds of monolayer cultures, Arsenic
(30–290 ppb) was capable of inhibiting the reformation of the epithelial
monolayer. An increase in activity and expression ofMMP-9 without increases of TIMP-1 protein expression was also observed
along with this alteration in wound repair. Furthermore, an improvement in
epithelial cell wound repair response was seen after inhibition of MMP-9 even
though the cells were exposed to 290 ppb arsenic. To conclude, arsenic is
capable of altering the airway epithelial barrier as arsenic induced increase in MMP-9/TIMP-1
ratio in lung epithelial cells can restrict proper wound repair.

MMP-9
expression has been associated with airway epithelial wound
repair in primary cultured cells and in vivo. Moreover, neutralizing MMP-9
using antibodies inhibited migration of HRECs indicating that MMP-9 was
important in cell migration during respiratory wound repair. Moreover, MMP-9
expression directly coincided with the speed of migration in HBECs. Therefore,
MMP-9 is normally upregulated in cells near the wound edge and in the presence
of arsenic, dysregulated wound repair was observed due to MMP-9 overexpression
in airway epithelial cells.

 

In the fibroblast model,
alterations in focal adhesion kinases, without a significant effect on actin
cytoskeleton rearrangements were observed at about 200 ppb arsenite. This
resulted in altered cell migration independent of MMP-9. There are also
contrasting reports showing that 750 ppb arsenic of unknown form alters actin
cytoskeleton and can lead to superoxide production and limit cell migration in
an endothelial cell line. In contrast with observations
that arsenite can inhibit migration,there are also reports that show arsenic
(37.5–375 ppb) in the form of arsenic trioxide (As2O3) can reduce carcinogenic
cell invasiveness in carcinogenic cell lines in part by downregulating MMP-9
(15, 46, 53)

 

 

Arsenic
Induces Cell Transformation at low concentrations and Apoptosis at Higher
Concentrations

Lower concentrations of
arsenite (0.5–25 ?M) exposure was capable of producing anchorage-independent
colonies of JB6 Cl 41 cells. But a higher concentration of arsenic (200 ?M)
induce apoptosis, thereby preventing the cells from undergoing transformation.

Differential
Activation of Erks and JNKs by Arsenite

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