AI Article Synopsis
- - The study focuses on Krüppel-like factor 3 (KLF3) and its role in lung cancer, showing that KLF3 levels are higher in lung cancer tissues and that reducing its expression hampers cancer cell growth and induces cell death.
- - Various assays were used to assess KLF3’s effect on cancer cell behavior, leading to findings that its knockdown limits cell proliferation, migration, and invasion while promoting apoptosis and halting the cell cycle.
- - The research identifies a regulatory pathway involving miR-326, Sp1, and KLF3, suggesting this axis could be a potential target for new lung cancer treatments.
Article Abstract
Objectives: To investigate the function and regulatory mechanism of Krüppel-like factor 3 (KLF3) in lung cancer.
Materials And Methods: KLF3 expression was analysed by qRT-PCR and Western blot assays. The proliferation, migration, invasion, cycle and apoptosis were measured by CCK-8 and EdU, wound-healing and Transwell, and flow cytometry assays. The tumour growth was detected by nude mouse tumorigenesis assay. In addition, the interaction between KLF3 and Sp1 was accessed by luciferase reporter, EMSA and ChIP assay. JAK2, STAT3, PI3K and p-AKT levels were evaluated by Western blot and IHC assays.
Results: The results indicated that KLF3 expression was elevated in lung cancer tissues. Knockdown of KLF3 inhibited lung cancer cell proliferation, migration and invasion, and induced cell cycle arrest and apoptosis. In addition, the downregulation of KLF3 suppressed tumour growth in vivo. KLF3 was transcriptionally activated by Sp1. miR-326 could bind to 3'UTR of Sp1 but not KLF3 and decreased the accumulation of Sp1, which further indirectly reduced KLF3 expression and inactivated JAK2/STAT3 and PI3K/AKT signaling pathways in vitro and in vivo.
Conclusions: Our data demonstrate that miR-326/Sp1/KLF3 regulatory axis is involved in the development of lung cancer, which hints the potential target for the further therapeutic strategy against lung cancer.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6495967 | PMC |
| http://dx.doi.org/10.1111/cpr.12551 | DOI Listing |
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