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
- Comprehensive Cancer Center research grant
- Fellinger Krebsforschungsverein
- Austrian Science Fund (FWF) [P 25599, P 32900, Doc 59-B33]
- Fund of City of Vienna for innovative, interdisciplinary cancer research
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available