Inhibition of Stat3 activation and tumor growth suppression of non-small cell lung cancer by G-quartet oligonucleotides
Open accessAbstract
Lung cancer is the leading cause of cancer mortality in the United States. Despite advances made over the past decades, the overall survival of patients with lung cancer remains dismal. Here we report novel G-quartet oligodeoxynucleotides (GQ-ODN) that were designed to selectively target signal transducer and activator of transcription 3 (Stat3), in the treatment of human non-small cell lung cancer (NSCLC). The objective of this study was to evaluate the effects of two novel GQ-ODN STAT3 inhibitors, T40214 and T40231, on NSCLC bearing nude mice. NSCLC bearing nude mice were assigned to 5 groups, which were treated by vehicle, control ODN, T40214, T40231, and Paclitaxel, respectively. Tumors were measured, isolated and analyzed using Western blotting, immuno-histochemistry, RPA and TUNEL. Results show that GQ-ODN T40214 and T40231 significantly suppress the growth of NSCLC tumors in nude mice by selectively inhibiting the activation of Stat3 and its downstream proteins Bcl-2, Bcl-xL, Mcl-1, survivin, VEGF, Cyclin D1 and c-myc; thereby, promoting apoptosis and reducing angiogenesis and cell proliferation. These findings validate Stat3 as an important molecular target for NSCLC therapy and demonstrate the efficacy of GQ-ODN in inhibiting Stat3 phosphorylation.
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Constitutive STAT3 signaling has been implicated in aberrant cell growth and proliferation in many cancers, including head and neck squamous cell carcinoma, colorectal carcinoma, melanoma, glioblastoma multiforme, multiple myeloma, non-small cell lung cancer, and others.
“Constitutive STAT3 signaling has been implicated in aberrant cell growth and proliferation in many cancers, including head and neck squamous cell carcinoma, colorectal carcinoma, melanoma, glioblastoma multiforme, multiple myeloma, non-small cell lung cancer, and others.58,69–73”
From Critical analysis of the potential for targeting STAT3 in human malignancy (2013) · cites this paper as [73]
The Introduction (page unavailable) says STAT3 contributes to oncogenesis and is constitutively activated in many human cancers, including head and neck and lung cancers. The Discussion specifically addresses non-small cell lung cancer. Our copy does not substantiate the sentence’s additional examples of colorectal carcinoma, melanoma, glioblastoma multiforme, or multiple myeloma. (LLM, conf=0.86)
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References 42 · Cited by 95
Research works printed but not linked: 2
- Stewart BW and Kleihues P: Lung Cancer. World Cancer Report. IARC Press, Lyon, France, 2003.
- Ginsberg RJ, Goldberg M and Waters PF: Surgery in non- small cell lung cancer. In: Thoracic Oncology. Roth JA RJ, Weisenburger TH (eds). 2nd edition. W.B. Saunders Company, Philadelphia, PA, pp124-126, 1995.
- Authors
- Weerasinghe, P., Garcia, G., Zhu, Q., Yuan, P., Feng, L., Mao, L., & Jing, N.
- Affiliations
- Baylor College of Medicine (US)
- The University of Texas MD Anderson Cancer Center (US)
- Venue
- International Journal of Oncology
- Publisher
- Spandidos Publications
- Published
- 2007-07-01
- Volume
- 31
- Issue
- 1
- Pages
- 129-36
- ISSN
- 1019-6439 (ISSN-L)
- 1791-2423
- OpenAlex
- W2057577723
- Cited by
- 95
- References
- 42
- Citations by year
- 2025: 3 · 2024: 2 · 2023: 4 · 2022: 5 · 2021: 4 · 2020: 1 · 2019: 10 · 2018: 3 · 2017: 5 · 2016: 7 · 2015: 10 · 2014: 5 · 2013: 6 · 2012: 7
- FWCI
- 2.53
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- International Journal of Oncology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Department of Defense (W81XWH)
- National Cancer Institute (CA-58204, R01CA104035, P50CA097007, P50CA058204, CA97007.)
- Topics
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA and Nucleic Acid Chemistry
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
- Keywords
- STAT3, non-small cell lung cancer, STAT3 inhibitor, tumor growth inhibition, apoptosis, angiogenesis, vascular endothelial growth factor, Bcl-2 family proteins, c-Myc, cyclin D1, STAT3 phosphorylation, paclitaxel
- MeSH terms
- Survivin, Animals, Carcinoma, Non-Small-Cell Lung, Immunohistochemistry, Lung Neoplasms, Mice, Nude, Microtubule-Associated Proteins, Neoplasm Proteins, Neovascularization, Pathologic, Oligodeoxyribonucleotides, Phosphorylation, Protein Conformation, Proto-Oncogene Proteins c-myc, Apoptosis, Paclitaxel, Proto-Oncogene Proteins c-bcl-2, Cyclin D1, Vascular Endothelial Growth Factor A, Cell Proliferation, STAT3 Transcription Factor, bcl-X Protein, Inhibitor of Apoptosis Proteins, Mice, Myeloid Cell Leukemia Sequence 1 Protein
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