ArticleCell & bioscience2021
KLF7/VPS35 axis contributes to hepatocellular carcinoma progression through CCDC85C-activated β-catenin pathway.
Article in Cell & bioscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 37 citations in OpenAlex.
- Targeting VPS35 increases chemotherapy sensitivity in gastric cancer cells via regulation of the NF-κB signaling pathway.Cancer gene therapy · 2026Article
- Retromer-targeted therapy for neurodegenerative diseases.Molecular neurodegeneration · 2026Review
- THBS1 upregulation by KLF7 in hypopharyngeal squamous cell carcinoma contributes to lung metastasis through the p38 MAPK signaling.iScience · 2026Article
- Comprehensive multi-omics analysis and experimental validation indicate that VPS35 is a promising biomarker for prognosis, immunotherapy, and chemotherapy in LIHC.RSC medicinal chemistry · 2026Article
- Vacuolar Protein Sorting 35 Controls Hepatocellular Proliferation Through SRC Signaling and Promotes Diethyl Nitrosamine-Induced Tumor Initiation.Cellular and molecular gastroenterology and hepatology · 2026Article
- Nuclear VPS35 attenuates NHEJ repair by sequestering Ku protein.Molecular medicine (Cambridge, Mass.) · 2025Article
- SNX17 mediates STAT3 activation to promote hepatocellular carcinoma progression via a retromer dependent mechanism.International journal of biological sciences · 2025Article
- Alterations of Krüppel-like Factor Signaling and Potential Targeted Therapy for Hepatocellular Carcinoma.Anti-cancer agents in medicinal chemistry · 2025Review
- VPS35-Retromer: Multifunctional Roles in Various Biological Processes - A Focus on Neurodegenerative Diseases and Cancer.Journal of inflammation research · 2025Review
- KLF7 enhances the invasion and migration of colorectal cancer cells via the miR-139-5p/TPD52 axis.Cancer biology & therapy · 2024Article
- Alpha-lipoic acid targetsActa biochimica et biophysica Sinica · 2024Article
- KLF7 Promotes Hepatocellular Carcinoma Progression Through Regulating SLC1A5-Mediated Tryptophan Metabolism.Journal of cellular and molecular medicine · 2024Article
- KLF7 reverses ox-LDL-induced ferroptosis in HMEC-1 cells through transcriptionally activating ALKBH5 to inhibit the m6A modification of ACSL4.Cytotechnology · 2024Article
- Palmitic acid promotes miRNA release from adipocyte exosomes by activating NF-κB/ER stress.Nutrition & diabetes · 2024Article
- Whole-genome de novo sequencing reveals genomic variants associated with differences of sex development in SRY negative pigs.Biology of sex differences · 2024Article
- Stable and oscillatory hypoxia differentially regulate invasibility of breast cancer associated fibroblasts.Mechanobiology in medicine · 2024Article
- KLF7 regulates super-enhancer-driven IGF2BP2 overexpression to promote the progression of head and neck squamous cell carcinoma.Journal of experimental & clinical cancer research : CR · 2024Article
- KLF7 promotes colon adenocarcinoma progression through the PDGFB signaling pathway.International journal of biological sciences · 2024Article
- Article
- New insights into KLFs and SOXs in cancer pathogenesis, stemness, and therapy.Seminars in cancer biology · 2023Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveDysregulation of KLF7 participates in the development of various cancers, but it is unclear whether there is a link between HCC and aberrant expression of KLF7. The aim of this study was to investigate the role of KLF7 in proliferation and migration of hepatocellular carcinoma (HCC) cells.
methodsCCK8, colony growth, transwell, cell cycle analysis and apoptosis detection were performed to explore the effect of KLF7, VPS35 and Ccdc85c on cell function in vitro. Xenografted tumor growth was used to assess in vivo role of KLF7. Chip-qPCR and luciferase reporter assays were applied to check whether KLF7 regulated VPS35 at transcriptional manner. Co-IP assay was performed to detect the interaction between VPS35 and Ccdc85c. Immunohistochemical staining and qRT-PCR analysis were performed in human HCC sampels to study the clinical significance of KLF7, VPS35 and β-catenin.
resultsFirstly, KLF7 was highly expressed in human HCC samples and correlated with patients' differentiation and metastasis status. KLF7 overexpression contributed to cell proliferation and invasion of HCC cells in vitro and in vivo. KLF7 transcriptional activation of VPS35 was necessary for HCC tumor growth and metastasis. Further, co-IP studies revealed that VPS35 could interact with Ccdc85c in HCC cells. Rescue assay confirmed that overexpression of VPS35 and knockdown of Ccdc85c abolished the VPS35-medicated promotion effect on cell proliferation and invasion. Finally, KLF7/VPS35 axis regulated Ccdc85c, which involved in activation of β-catenin signaling pathway, confirmed using β-catenin inhibitor, GK974. Functional studies suggested that downregulation of Ccdc85c partly reversed the capacity of cell proliferation and invasion in HCC cells, which was regulated by VPS35 upregulation. Lastly, there was a positive correlation among KLF7, VPS35 and active-β-catenin in human HCC patients.
conclusionWe demonstrated that KLF7/VPS35 axis promoted HCC cell progression by activating Ccdc85c-medicated β-catenin pathway. Targeting this signal axis might be a potential treatment strategy for HCC.
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