4.6 Review

STAT3: Versatile Functions in Non-Small Cell Lung Cancer

Journal

CANCERS
Volume 12, Issue 5, Pages -

Publisher

MDPI
DOI: 10.3390/cancers12051107

Keywords

signal transducer and activator of transcription (STAT); Janus kinase (JAK); cytokines; interleukin (IL); non-small cell lung cancer (NSCLC); lung adenocarcinoma (AC); Kirsten rat sarcoma viral proto-oncogene (K-RAS); epidermal growth factor receptor (EGFR); tumor microenvironment (TME); tumor-promoting inflammation; anti-tumor immunity; clinical trials

Categories

Funding

  1. Comprehensive Cancer Center research grant
  2. Fellinger Krebsforschungsverein
  3. Austrian Science Fund (FWF) [P 25599, P 32900, Doc 59-B33]
  4. Fund of City of Vienna for innovative, interdisciplinary cancer research

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Signal Transducer and Activator of Transcription 3 (STAT3) activation is frequently found in non-small cell lung cancer (NSCLC) patient samples/cell lines and STAT3 inhibition in NSCLC cell lines markedly impairs their survival. STAT3 also plays a pivotal role in driving tumor-promoting inflammation and evasion of anti-tumor immunity. Consequently, targeting STAT3 either directly or by inhibition of upstream regulators such as Interleukin-6 (IL-6) or Janus kinase 1/2 (JAK1/2) is considered as a promising treatment strategy for the management of NSCLC. In contrast, some studies also report STAT3 being a tumor suppressor in a variety of solid malignancies, including lung cancer. Here, we provide a concise overview of STAT3's versatile roles in NSCLC and discuss the yins and yangs of STAT3 targeting therapies.

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