ArticleTranslational oncology2022
KLF4 suppresses the proliferation and metastasis of NSCLC cells via inhibition of MSI2 and regulation of the JAK/STAT3 signaling pathway.
Article in Translational oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Regulatory Role of Zinc in Acute Promyelocytic Leukemia: Cellular and Molecular Aspects with Therapeutic Implications.International journal of molecular sciences · 2025Review
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- Epithelial zinc finger protein in lung adenocarcinoma: prognostic biomarker with molecular and clinical implications.Hereditas · 2025Article
- ITGB5 as a Potential Diagnostic Biomarker for Osteoarthritis.Journal of musculoskeletal & neuronal interactions · 2025Article
- Targeting STAT3 signaling pathway by curcumin and its analogues for breast cancer: A narrative review.Animal models and experimental medicine · 2024Review
- Therapeutic Targeting of Krüppel-Like Factor 4 and Its Pharmacological Potential in Parkinson's Disease: a Comprehensive Review.Molecular neurobiology · 2024Review
- Review
- Sparse Independence Component Analysis for Competitive Endogenous RNA Co-Module Identification in Liver Hepatocellular Carcinoma.IEEE journal of translational engineering in health and medicine · 2023Article
- Fucoxanthin suppresses the malignant progression of ovarian cancer by inactivating STAT3/c-Myc signaling.American journal of translational research · 2023Article
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNon-small cell lung cancer (NSCLC) remains an aggresive tumor with poor survival rates. Krüppel-like factor 4 (KLF4) is known to be involved in progression of NSCLC; however, the detailed mechanism by which KLF4 regulates the progression of NSCLC remains unclear.
methodsIn order to investigate the function of KLF4 in NSCLC, cell proliferation was measured by MTT and colony formation assays. The migration and invasion of NSCLC cells were detected via wound healing and Transwell assays, respectively. Then, the interaction between KLF4 and MSI2 was confirmed using a dual-luciferase reporter assay, and the mechanism by which KLF4 regulates the tumorigenesis of NSCLC was assessed by RT-qPCR and Western blotting.
resultsThe results showed that KLF4 was downregulated, while MSI2 was upregulated in NSCLC. Additionally, KLF4 could inhibit transcription of MSI2, and overexpression of KLF4 or knockdown of MSI2 could inhibit the proliferation, migration and invasion of NSCLC cells. Moreover, KLF4 could inhibit JAK2/STAT3 signalling pathway.
conclusionsIn conclusion, KLF4 significantly inhibited the proliferation, invasion and migration of NSCLC cells via inactivation of MSI2/JAK2/STAT3 signalling pathway. Thereby, our finding might shed new lights on exploring the new strategies against NSCLC.
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