ArticleJournal of cancer research and clinical oncology2011
Down-regulation of JAK1 by RNA interference inhibits growth of the lung cancer cell line A549 and interferes with the PI3K/mTOR pathway.
Article in Journal of cancer research and clinical oncology, 2011. 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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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Non-coding RNAs as key regulators of epithelial-mesenchymal transition in breast cancer.Frontiers in cell and developmental biology · 2025Review
- CTDSPL2 promotes the progression of non-small lung cancer through PI3K/AKT signaling via JAK1.Cell death discovery · 2024Article
- Essential contribution of the JAK/STAT pathway to carcinogenesis, lytic infection of herpesviruses and pathogenesis of COVID‑19 (Review).Molecular medicine reports · 2024Review
- Inhibition of Janus Kinase 1 synergizes docetaxel sensitivity in prostate cancer cells.Journal of cellular and molecular medicine · 2021Article
- Decreased expression of JAK1 associated with immune infiltration and poor prognosis in lung adenocarcinoma.Aging · 2020Article
- Review
- miR-140-3p inhibits progression of non-small cell lung cancer by targeting Janus kinase 1.Journal of biosciences · 2020Article
- STAT3-Induced Wnt5a Provides Chronic Lymphocytic Leukemia Cells with Survival Advantage.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- The Upregulation of Toll-Like Receptor 3 via Autocrine IFN-β Signaling Drives the Senescence of Human Umbilical Cord Blood-Derived Mesenchymal Stem Cells Through JAK1.Frontiers in immunology · 2019Article
- Ginsenoside Rh2 epigenetically regulates cell-mediated immune pathway to inhibit proliferation of MCF-7 breast cancer cells.Journal of ginseng research · 2018Article
- STAT3 is constitutively acetylated on lysine 685 residues in chronic lymphocytic leukemia cells.Oncotarget · 2018Article
- Activation of Janus kinase 1 confers poor prognosis in patients with non-small cell lung cancer.Oncology letters · 2017Article
- EGFR and KRAS mutations do not enrich for the activation of IL-6, JAK1 or phosphorylated STAT3 in resected lung adenocarcinoma.Medical oncology (Northwood, London, England) · 2017Article
- Constitutive Phosphorylation of STAT3 by the CK2-BLNK-CD5 Complex.Molecular cancer research : MCR · 2017Article
- Article
- BAD overexpression inhibits cell growth and induces apoptosis via mitochondrial-dependent pathway in non-small cell lung cancer.Cancer cell international · 2013Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeThe mammalian Janus kinase (JAK) family plays a critical role in cytokine/growth factor signalling pathways and is associated with human cancers. In this study, we explored the role of JAK1 in the non-small cell lung cancer (NSCLC) cell line A549 and its molecular crosstalk with the phosphatidyl inositol-3-kinase (PI3K)/mammalian target of the rapamycin (mTOR) pathway.
methodsOne hundred and two NSCLC and 50 normal lung specimens were collected after surgical resection. JAK1 expression and phosphorylation were determined via immunohistochemical staining (IHC) assay. A stable knockdown of JAK1 was performed in A549 cells by RNA interference. Stable cell proliferation, cell cycle, apoptosis, and invasion were characterised in vitro. Tumourigenicity was analysed in vivo. The NSCLC xenograft protein expression of PI3K/mTOR pathway molecules was determined by Western blot assay.
resultsJAK1 expression was higher in NSCLC tissues than in normal lung tissues (P < 0.01). JAK1 knockdown in A549 cells significantly inhibited cell proliferation and invasion while promoting cell arrest at G0/G1 phase (all P < 0.05). The xenograft model showed that JAK1 suppression inhibited tumour growth compared with normal control (P < 0.05). Moreover, JAK1 knockdown inhibited mTOR or P70 ribosomal protein S6 kinase (P70S6K) phosphorylation, but increased glycogen synthase kinase-3α (GSK-3α) and B-cell lymphoma-extra large (Bcl-xl) phosphorylation. Total protein expression and Akt1/2 phosphorylated status remained unchanged.
conclusionOur study suggests that JAK1 expression and phosphorylation is abnormal in NSCLC tissues. The knockdown of JAK1 significantly inhibits tumourigenicity of the A549 cell line and demonstrates that crosstalk between the JAK1 and PI3K/mTOR pathways is involved.
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