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Enhancing chemotherapy efficacy in Pten-deficient prostate tumors by activating the senescence-associated antitumor immunity. | LitMetric

AI Article Synopsis

  • - Prosenescence therapy is a new cancer treatment strategy, but its effectiveness is debated due to conflicting evidence about the effects of senescent tumor cells.
  • - In tumors lacking the Pten gene, the Jak2/Stat3 signaling pathway creates an environment that suppresses the immune response, aiding tumor growth and making them resistant to chemotherapy.
  • - Combining the chemotherapy drug docetaxel with a JAK2 inhibitor can enhance the immune response against tumors and improve treatment outcomes by reprogramming the cancer-related secretions from senescent cells.

Article Abstract

Prosenescence therapy has recently emerged as a novel therapeutic approach for treating cancer. However, this concept is challenged by conflicting evidence showing that the senescence-associated secretory phenotype (SASP) of senescent tumor cells can have pro- as well as antitumorigenic effects. Herein, we report that, in Pten-null senescent tumors, activation of the Jak2/Stat3 pathway establishes an immunosuppressive tumor microenvironment that contributes to tumor growth and chemoresistance. Activation of the Jak2/Stat3 pathway in Pten-null tumors is sustained by the downregulation of the protein tyrosine phosphatase PTPN11/SHP2, providing evidence for the existence of a novel PTEN/SHP2 axis. Importantly, treatment with docetaxel in combination with a JAK2 inhibitor reprograms the SASP and improves the efficacy of docetaxel-induced senescence by triggering a strong antitumor immune response in Pten-null tumors. Altogether, these data demonstrate that immune surveillance of senescent tumor cells can be suppressed in specific genetic backgrounds but also evoked by pharmacological treatments.

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Source
http://dx.doi.org/10.1016/j.celrep.2014.08.044DOI Listing

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