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Polishchuk, V.

Publications and source records attributed to Polishchuk, V..

2 recordsLinked to original sources

Differential Expression of TKS4 Isoforms and Their Role in Cellular Processes in Breast Cancer

The scaffold protein TKS4 plays a role in the development of several cancers. Alternative splicing of the TKS4 gene generates two isoforms, TKS4L and TKS4b; however, their distinct expression patterns and functional roles have not yet been characterized. We have shown that TKS4 isoforms were differentially expressed across human cell lines and breast cancer (BC) tumor samples. Both TKS4L and TKS4L/TKS4b mRNA ratios were significantly altered in tumors compared with adjacent tissues. We identified six novel binding SH3-domain-containing partners for TKS4L, none of which interact with TKS4b, suggesting their functional differences. Tyrosine phosphorylation of both isoforms was induced by Src(Y527F) kinase overexpression, enabling binding to the SH2 domains of signaling proteins. Interestingly, TKS4b significantly accumulated in the nucleus, while TKS4L was primarily present in the cytosol in MCF-7 cells. TKS4b overexpression enhanced MCF-7 cell migration. Both TKS4 isoforms exhibit oncogenic properties by promoting epithelial-mesenchymal transition in BC cells, highlighting their potential as targets for therapeutic intervention.

molecular biology↗

A bioenergetic basis for multiorgan dysfunction in sepsis

Sepsis is a life-threatening multiorgan dysfunction that develops from a maladaptive host response to infection1. With an estimated 49 million cases per year and [~]11 million related deaths2, sepsis is a global WHO health priority3. Failure to overcome sepsis morbidity and lethality4,5 calls for alternative therapeutic approaches6-8. Here we report that adipocyte lipolysis is vital to prevent the pathogenesis of sepsis in mice. This protective response is evolutionary conserved, producing a plasma lipidomic profile9,10 that reflects on the severity of clinical sepsis. Mechanistically, adipocyte lipolysis fuels energy metabolism to sustain adaptive thermoregulation to infection, via insulin production and insulin receptor (INSR) signaling in adipocytes. This metabolic-based defense strategy does not impact on bacterial burden, establishing disease tolerance to infection11-14. In conclusion, adipocyte lipolysis induces insulin to rewire energy metabolism and support organ function in response to infection.

pathology↗