ArticleOncotarget2017
ING5 knockdown enhances migration and invasion of lung cancer cells by inducing EMT via EGFR/PI3K/Akt and IL-6/STAT3 signaling pathways.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 64 citations in OpenAlex.
- OverlappING and DivergING roles of ING4 and ING5 in cancer, differentiation and development.Frontiers in cell and developmental biology · 2026Review
- ING5: multifaceted roles beyond tumor suppression in cellular physiology and disease.Epigenetics & chromatin · 2025Review
- microRNA-196b-5p expression in cancer tissues is closely associated with clinical and pathological characteristics and prognosis of patients with non-small cell lung cancer.Journal of cardiothoracic surgery · 2025Article
- Interleukin-9 promotes EMT-mediated PMArchives of toxicology · 2024Article
- ING5 inhibits aerobic glycolysis of lung cancer cells by promoting TIE1-mediated phosphorylation of pyruvate dehydrogenase kinase 1 at Y163.Frontiers of medicine · 2024Article
- PI3K/AKT pathway as a pivotal regulator of epithelial-mesenchymal transition in lung tumor cells.Cancer cell international · 2024Review
- ING5 overexpression upregulates miR-34c-5p/Snail1 to inhibit EMT and invasion of lung cancer cells.Acta biochimica et biophysica Sinica · 2023Article
- Non-small cell lung carcinoma (NSCLC): Implications on molecular pathology and advances in early diagnostics and therapeutics.Genes & diseases · 2023Review
- Interplay of broccoli/broccoli sprout bioactives with gut microbiota in reducing inflammation in inflammatory bowel diseases.The Journal of nutritional biochemistry · 2023Review
- Mutational Damages in Malignant Lung Tumors.Asian Pacific journal of cancer prevention : APJCP · 2023Article
- 3-Nitrobenzanthrone promotes malignant transformation in human lung epithelial cells through the epiregulin-signaling pathway.Cell biology and toxicology · 2022Article
- Molecular mechanisms of inhibitor of growth (ING) family members in health and malignancy.Cancer cell international · 2022Review
- The roles of ING5 in cancer: A tumor suppressor.Frontiers in cell and developmental biology · 2022Review
- Transcriptional Regulation of ING5 and its Suppressive Effects on Gastric Cancer.Frontiers in oncology · 2022Article
- Therapeutic advances in non-small cell lung cancer: Focus on clinical development of targeted therapy and immunotherapy.MedComm · 2021Review
- Review
- Overexpression ofExperimental and therapeutic medicine · 2021Article
- Pepsin Promotes Activation of Epidermal Growth Factor Receptor and Downstream Oncogenic Pathways, at Slightly Acidic and Neutral pH, in Exposed Hypopharyngeal Cells.International journal of molecular sciences · 2021Article
- Review
- MicroRNA-196b-5p promotes malignant progression of colorectal cancer by targeting ING5.Cancer cell international · 2020Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ING5 belongs to the Inhibitor of Growth (ING) candidate tumor suppressor family, whose functions have been involved in the regulation of chromatin remodeling, cell cycle progression, proliferation and apoptosis. Our previous study has shown that ING5 overexpression inhibits lung cancer aggressiveness via suppressing epithelial to mesenchymal transition (EMT). However, the mechanisms remain largely unknown. In the current study, by Phospho-Kinase array and western blot, we have defined significantly upregulated EGFR/PI3K/Akt and IL-6/STAT3 oncogenic signaling pathways in ING5 knockdown A549 cells, which could be downregulated by ING5 overexpression. PI3K inhibitor ZSTK474 or STAT3 inhibitor Niclosamide not only abolished ING5 knockdown-promoted proliferation, colony formation, migration and invasion of lung cancer A549 cells, but also impaired ING5 knockdown-stimulated metastasis of cancer cells in mouse xenograft models with tail vein injection of A549 cells. Furthermore, treatment with ZSTK474 or Niclosamide decreased protein level of EGFR, p-Akt, IL-6 and p-STAT3, and reversed ING5 knockdown-promoted EMT, as indicated by downregulated expression of EMT marker E-cadherin, an epithelial marker, increased expression of N-cadherin, a mesenchymal marker, and EMT-related transcription factors including Snail, Slug, Smad3 and Twist. Taken together, these results demonstrate that loss of ING5 enhances aggressiveness of lung cancer cells by promoting EMT via activation of EGFR/PI3K/Akt and IL-6/STAT3 signaling pathways.
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