Stat3 inhibits Beclin 1 expression through recruitment of HDAC3 in nonsmall cell lung cancer cells
Abstract
Recent studies have shown that Beclin 1, a key regulator of autophagic process, is frequently downregulated and may serve as an independent prognostic biomarker for nonsmall cell lung cancer. However, the molecular mechanisms underlying its downregulation remain poorly understood. The signal transducer and activator of transcription 3 (Stat3) is a transcription factor which plays a crucial role for multiple tumor growth and progression. Here, we demonstrate that Beclin 1 is a direct transcriptional target of Stat3 in lung cancer cells. Interleukin-6 (IL-6) treatment or transfection of a constitutively activated Stat3 in AGS and NCI-H1650 cells inhibited Beclin 1 expression. At the molecular level, we further revealed that Stat3 could directly bind to the promoter region of Beclin 1 and repressed its transcription through recruiting histone deacetylase 3 (HDAC3). Collectively, our results suggest that the activated Stat3 may represent an important mechanism for Beclin 1 downregulation in nonsmall cell lung cancer development.
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STAT3 negatively regulates both PIK3C3 and BECN1 through recruitment of HDAC3 on its promoter.
“STAT3 also negatively regulates both PIK3C3 (Yamada et al., 2012) and BECN1 (Miao et al., 2014) through recruitment of HDAC3 on its promoter (Miao et al., 2014).”
From Targeting Janus Kinases and Signal Transducer and Activator of Transcription 3 To Treat Inflammation, Fibrosis, and Cancer: Rationale, Progress, and Caution (2020) · cites this paper as Miao et al., 2014
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Yue, Z., Jin, S., Yang, C., Levine, A. J., & Heintz, N. (2003) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2436255100 · Cited by 2,116 · see citing works
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Targeting epigenetic regulators for cancer therapy: mechanisms and advances in clinical trials
Cheng, Y., He, C., Wang, M., Ma, X., Mo, F., Yang, S., Han, J., & Wei, X. (2019) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-019-0095-0 · Cited by 1,097 · see citing works
The role of STAT3 in autophagy
You, L., Wang, Z., Li, H., Shou, J., Jing, Z., Xie, J., Sui, X., Pan, H., & Han, W. (2015) · Autophagy · doi:10.1080/15548627.2015.1017192 · Cited by 515 · see citing works
Bharadwaj, U., Kasembeli, M. M., Robinson, P., & Tweardy, D. J. (2020) · Pharmacological Reviews · doi:10.1124/pr.119.018440 · Cited by 314 · see citing works
“, 2012) and BECN1 (Miao et al., 2014) through recruitment of HDAC3 on its promoter (Miao et al.”
BackgroundInfluentialHistone deacetylase 3 (HDAC3) inhibitors as anticancer agents: A review
Sarkar, R., Banerjee, S., Amin, S. A., Adhikari, N., & Jha, T. (2020) · European Journal of Medicinal Chemistry · doi:10.1016/j.ejmech.2020.112171 · Cited by 121 · see citing works
- Authors
- Miao, L.-J., Huang, F.-X., Sun, Z.-T., Zhang, R.-X., Huang, S.-F., & Wang, J.
- Affiliations
- First Affiliated Hospital of Zhengzhou University (CN)
- Corresponding author
- Wang, Jing
- Venue
- Tumor Biology
- Published
- 2014-04-24
- Volume
- 35
- Issue
- 7
- Pages
- 7097-7103
- ISSN
- 1010-4283 (ISSN-L)
- 1423-0380
- OpenAlex
- W2080844733
- Cited by
- 62
- References
- 1
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 4 · 2023: 5 · 2022: 8 · 2021: 2 · 2020: 12 · 2019: 9 · 2018: 7 · 2017: 2 · 2015: 5 · 2014: 2
- FWCI
- 1.45
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Tumor Biology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Keywords
- STAT3, Beclin-1, HDAC3, non-small cell lung cancer, autophagy, transcriptional repression, interleukin-6, promoter binding, gene downregulation, prognostic factors
- MeSH terms
- Beclin-1, Histone Deacetylase 3, Carcinoma, Non-Small-Cell Lung, Histone Deacetylases, Humans, Membrane Proteins, Promoter Regions, Genetic, Signal Transduction, Interleukin-6, Gene Expression Regulation, Neoplastic, Cell Line, Tumor, STAT3 Transcription Factor, Apoptosis Regulatory Proteins
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