The role of STAT3 in leading the crosstalk between human cancers and the immune system.

Cancer Lett

Department of Maxillofacial and Otorhinolaryngological Oncology, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, China; Key Laboratory of Cancer Prevention and Therapy, Tianjin Cancer Institute, Tianjin 300060, China; National Clinical Research Center of Cancer, Tianjin 300060, China. Electronic address:

Published: February 2018

AI Article Synopsis

  • Cancers develop through a mix of internal and external factors, with STAT3 playing a key role by being constantly active in both tumor cells and immune cells.
  • When activated, STAT3 promotes tumor growth by regulating genes that support cancer and suppressing immune responses, leading to a more favorable environment for tumors.
  • Research suggests that targeting STAT3 could boost the body's immune response against cancer and improve the immune environment in tumors, making it a potential focus for cancer treatment strategies.

Article Abstract

The development and progression of human cancers are continuously and dynamically regulated by intrinsic and extrinsic factors. As a converging point of multiple oncogenic pathways, signal transducer and activator of transcription 3 (STAT3) is constitutively activated both in tumor cells and tumor-infiltrated immune cells. Activated STAT3 persistently triggers tumor progression through direct regulation of oncogenic gene expression. Apart from its oncogenic role in regulating gene expression in tumor cells, STAT3 also paves the way for human cancer growth through immunosuppression. Activated STAT3 in immune cells results in inhibition of immune mediators and promotion of immunosuppressive factors. Therefore, STAT3 modulates the interaction between tumor cells and host immunity. Accumulating evidence suggests that targeting STAT3 may enhance anti-cancer immune responses and rescue the suppressed immunologic microenvironment in tumors. Taken together, STAT3 has emerged as a promising target in cancer immunotherapy.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5748258PMC
http://dx.doi.org/10.1016/j.canlet.2017.12.003DOI Listing

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