Abstract
Bacteria is recognized as opportunistic tumor inhabitant, giving rise to an environmental stress that may alter tumor microenvironment, which directs cancer behavior. In vitro infection of the T24 cell line with E. coli was performed to study the bacterial impact on bladder cancer cells. EMT markers were assessed using immunohistochemistry, western blot and RT-PCR. Stemness characteristics were monitored using RT-PCR. Furthermore, the metabolic reprograming was investigated by detection of ROS and metabolic markers. A significant (p ≤ 0.001) upregulation of vimentin as well as downregulation of CK19 transcription and protein levels was reported. A significant increase (p ≤ 0.001) in the expression level of stemness markers (CD44, NANOG, SOX2 and OCT4) was reported. ROS level was elevated, that led to a significant increase (p ≤ 0.001) in UCP2. This enhanced a significant increase (p ≤ 0.001) in PDK1 to significantly downregulate PDH (p ≤ 0.001) in order to block oxidative phosphorylation in favor of glycolysis. This resulted in a significant decrease (p ≤ 0.001) of AMPK, and a significant elevation (p ≤ 0.001) of MCT1 to export the produced lactate to extracellular matrix. Thus, bacteria may induce alteration to the heterogonous tumor cell population through EMT, CSCs and metabolic reprogramming, which may improve cancer cell ability to migrate and self-renew.
Highlights
Bacteria is recognized as opportunistic tumor inhabitant, giving rise to an environmental stress that may alter tumor microenvironment, which directs cancer behavior
Understanding the mechanism by which bacteria influence tumor environment may facilitate solving the mystery of cancer progression and help therapy development
The master characteristic of epithelial mesenchymal transition (EMT) is the activation of some transcription factors that lead to increase of mesenchymal-related proteins in advance of epithelial ones
Summary
Bacteria is recognized as opportunistic tumor inhabitant, giving rise to an environmental stress that may alter tumor microenvironment, which directs cancer behavior. Bacteria may induce alteration to the heterogonous tumor cell population through EMT, CSCs and metabolic reprogramming, which may improve cancer cell ability to migrate and self-renew. Epithelial cells may undergo EMT, which is a physiological phenotypic shift that endows epithelial cancer cell with mesenchymal features and downs epithelial characteristics, in order to acquire static cancer cell the ability of migration and invasion. This process occurs naturally during wound healing and embryogenesis, while accumulating evidence has pointed it out as a central driver of cancer m etastasis[3,6]. Cells with CSCs features possess higher resistance to chemotherapies and cause tumor d ormancy[9]
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