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Cited by 511Cytokine Signaling Pathways and InteractionsCancer Mechanisms and TherapyTGF-β signaling in diseases

STAT3 Target Genes Relevant to Human Cancers

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Carpenter, Richard, Lo, Hui-Wen·2014·Cancers
DOI 10.3390/cancers6020897PMC PMC4074809
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Abstract

Since its discovery, the STAT3 transcription factor has been extensively studied for its function as a transcriptional regulator and its role as a mediator of development, normal physiology, and pathology of many diseases, including cancers. These efforts have uncovered an array of genes that can be positively and negatively regulated by STAT3, alone and in cooperation with other transcription factors. Through regulating gene expression, STAT3 has been demonstrated to play a pivotal role in many cellular processes including oncogenesis, tumor growth and progression, and stemness. Interestingly, recent studies suggest that STAT3 may behave as a tumor suppressor by activating expression of genes known to inhibit tumorigenesis. Additional evidence suggested that STAT3 may elicit opposing effects depending on cellular context and tumor types. These mixed results signify the need for a deeper understanding of STAT3, including its upstream regulators, parallel transcription co-regulators, and downstream target genes. To help facilitate fulfilling this unmet need, this review will be primarily focused on STAT3 downstream target genes that have been validated to associate with tumorigenesis and/or malignant biology of human cancers.

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  • Aberrant STAT3 activation has been implicated in tumor initiation and progression, and preclinical evidence supports STAT3 as a potential treatment target in STAT3-dependent epithelial cancer.

    “Aberrant STAT3 activation has been implicated in tumor initiation and progression, and preclinical evidence strongly supports STAT3 as a potential treatment target in STAT3-dependent epithelial cancer (1, 3, 46).”

    From Small-molecule PROTAC mediates targeted protein degradation to treat STAT3-dependent epithelial cancer (2022) · cites this paper as [1]

    The Introduction links STAT3 activation to oncogenesis and tumor progression, and the Conclusions describe efforts to develop STAT3-targeted therapies. The paper does not specifically state that strong preclinical evidence supports treatment of STAT3-dependent epithelial cancer; it also cautions that STAT3’s role depends on tumor type and cellular context. (LLM, conf=0.83)

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Cited by

Sorted by citations

Authors
Carpenter, R., & Lo, H.-W.
Affiliations
Duke University (US)
Corresponding author
Lo, Hui-Wen
ORCID
Venue
Cancers
Publisher
MDPI AG
Published
2014-04-16
Volume
6
Issue
2
Pages
897-925
ISSN
2072-6694 (ISSN-L)
DOI
10.3390/cancers6020897
PMC
PMC4074809
OpenAlex
W2143819289
Cited by
511
References
7
Citations by year
2026: 22 · 2025: 32 · 2024: 36 · 2023: 46 · 2022: 66 · 2021: 60 · 2020: 57 · 2019: 45 · 2018: 40 · 2017: 40 · 2016: 35 · 2015: 27 · 2014: 5
FWCI
17.23
Type
journal article
Language
en
Open access
Licence
Locations
  • Cancers (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
Funders
  • National Institutes of Health (W81XWH)
  • National Cancer Institute (K01CA118423)
  • National Institute of Neurological Disorders and Stroke (R01NS087169)
Topics
  • Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Cancer Mechanisms and Therapy
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
Keywords
STAT3, downstream target genes, transcriptional regulation, carcinogenesis, tumor growth and progression, cancer stemness, tumor suppressor function, upstream regulators, human cancer

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