ArticleCancer biology & therapy2019
Krüppel like factor 6 splice variant 1 (KLF6-SV1) overexpression recruits macrophages to participate in lung cancer metastasis by up-regulating TWIST1.
Article in Cancer biology & therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 19 citations in OpenAlex.
- Reprogramming the tumor microenvironment via TFF3 targeting: a potential novel avenue to boost CAR-T cell therapy in solid tumors.Cancer gene therapy · 2026Review
- The CCL2-CCR2 axis in primary lung cancer and pulmonary metastasis: from molecular mechanisms to therapeutic potentials.Frontiers in immunology · 2026Review
- Pharmacological and toxicological roles of Kruppel-like factors (KLFs) in the cardiovascular system: a review.Molecular biology reports · 2025Review
- The role and clinical significance of tumor-associated macrophages in the epithelial-mesenchymal transition of lung cancer.Frontiers in oncology · 2025Review
- Cancer stem cells: advances in knowledge and implications for cancer therapy.Signal transduction and targeted therapy · 2024Review
- Abnormal expression of Krüppel-like transcription factors and their potential values in lung cancer.Heliyon · 2024Review
- Tumor-associated macrophages: an effective player of the tumor microenvironment.Frontiers in immunology · 2023Review
- Krüppel-like factors in tumors: Key regulators and therapeutic avenues.Frontiers in oncology · 2023Review
- Targeting tumor-associated macrophage: an adjuvant strategy for lung cancer therapy.Frontiers in immunology · 2023Review
- Macrophages Are a Double-Edged Sword: Molecular Crosstalk between Tumor-Associated Macrophages and Cancer Stem Cells.Biomolecules · 2022Review
- Roles of Krüppel-like factor 6 splice variant 1 in the development, diagnosis, and possible treatment strategies for non-small cell lung cancer.American journal of cancer research · 2022Review
- Exosomal miR-487a derived from m2 macrophage promotes the progression of gastric cancer.Cell cycle (Georgetown, Tex.) · 2021Article
- CCL2: An Important Mediator Between Tumor Cells and Host Cells in Tumor Microenvironment.Frontiers in oncology · 2021Review
- Krüppel-Like Factor 6 Splice Variant 1: An Oncogenic Transcription Factor Involved in the Progression of Multiple Malignant Tumors.Frontiers in cell and developmental biology · 2021Review
- Identification and Validation of a Stromal EMT Related LncRNA Signature as a Potential Marker to Predict Bladder Cancer Outcome.Frontiers in oncology · 2021Article
- Effect of apigenin on whole transcriptome profile of TNFα-activated MDA-MB-468 triple negative breast cancer cells.Oncology letters · 2020Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of this study was to investigate the mechanism by which KLF6-SV1 promoted lung cancer metastasis through tumor-associated macrophages (TAMs). Plasmid transfection was used to construct cells that upregulated or silenced gene. Tumor-bearing mouse model was established using A549 cells. SP staining was performed to detect the CD163 and CD68. Six-well plates and Transwell chamber were used for co-culture of lung cancer A549 cells and macrophages. CCK-8 and Transwell assay were applied to detected the cell viability and migration respectively. Protein and mRNA were tested by Western blot and quantitative real-time polymerase chain reaction (qRT-PCR).KLF6-SV1 overexpression promoted the expression levels of TWIST1 and CCL2, and also induce macrophage polarization to M2 and epithelial-mesenchymal transition (EMT). In vitro experiments showed that KLF6-SV1 might regulate the migration of lung cancer cells by regulating the expression of TWIST1 and CCL-2. M2 macrophages did not affect the expression of KLF6-SV1, TWIST1 and CCL-2. The co-culture system could up-regulate the EMT of A549 cells.Overexpression of KLF6-SV1 promoted the expression of TWIST1 and CCL2, and up-regulation of TWIST1 expression might promote the infiltration of M2 macrophages, which promoted the involvement of EMT in the metastasis of lung cancer cells.
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