onsdag 27 november 2019

Ny forskningsrapport från Polen

7 forskare från polska Jagiellonian University har fått sina studier om magcancer (gastric cancer) granskade,godkända och publicerade i det vetenskapliga organet Spandidos Publications.
Igår 26/11 i deras edition International Journal of Oncology närmare bestämt.




Autologous tumor‑derived microvesicles influence gene expression profiles and enhance protumorigenic chemotactic potential, signal transduction and cellular respiration in gastric cancer cells

  • Published online on: November 26, 2019     https://doi.org/10.3892/ijo.2019.4923

Ur abstractet får vi info att man använt sig av HoloMonitor.

 

Abstract


Tumor‑derived microvesicles (TMVs) interact with a variety of different cell types within the immune system, including lymphocytes, monocytes, dendritic cells and tumor cells that they have originated from. 
In the present study, the effects of autologous‑TMVs (auto‑TMVs) on gene expression, chemotaxis, intercellular signaling and cellular metabolism were examined in cells of the gastric cancer (GC) cell line 1415 (GC1415). 
The effects of auto‑TMVs on mRNA gene expression in GC1415 cells were assessed using pathway‑focused PCR arrays. 
A chemotaxis assay was performed using the HoloMonitor M4 System
Signaling pathways were evaluated using western blot analysis, and cellular respiration was measured using the Seahorse XF Cell Mito Stress Test. 
Exposure of the GC1415 cells to auto‑TMVs led to the overexpression (75 genes) and underexpression (96 genes) of genes that are associated with signal transduction, metabolism, chemotaxis, angiogenesis and metastasis. 
The auto‑TMVs were indicated to induce chemotaxis and activate the PI3K/AKT signaling pathway in GC1415 cells. 
However, the MAPK/ERK signaling pathway was not indicated to be activated. 
Furthermore, studies on cellular respiration in GC1415 cells exposed to auto‑TMVs demonstrated a metabolic shift to glycolysis. 
The results of the current study thus indicate that auto‑TMVs may exert an effect on tumor cell function.

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