ArticleCancers2019
JAK2 Inhibition Impairs Proliferation and Sensitises Cervical Cancer Cells to Cisplatin-Induced Cell Death.
Article in Cancers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
43 citing papers in PubMed, 60 citations in OpenAlex.
- Integrating QSAR-Machine Learning, Biochemical Assays, and Molecular Dynamics for the Discovery of JAK2 Inhibitors in Cervical Cancer.Journal of chemical information and modeling · 2026Article
- Hypoxia promotes progression of cervical cancer by modulating the ATXN3-enhanced P53 stability or STAT5 phosphorylation.Cell death discovery · 2026Article
- A mitochondrial regulatory network of ferroptosis defense in HPV-positive cervical cancer: therapeutic implications of the mitoSTAT3-DHODH axis.Frontiers in pharmacology · 2026Review
- Identification of Novel JAK2 Inhibitors from Amino Derivatives of Epoxyalantolactone: In Silico and In Vitro Studies.International journal of molecular sciences · 2025Article
- [Therapeutic mechanism of hederagenin, an active component inNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- Astragalin inhibits the proliferation of high-risk HPV-positive cervical epithelial cells and attenuates malignant cervical lesions.Cytotechnology · 2025Article
- Exploring novel furochochicine derivatives as promising JAK2 inhibitors in HeLa cells: Integrating docking, QSAR-ML, MD simulations, and experiments.Computational and structural biotechnology journal · 2025Article
- Navigating the Molecular Signaling: Deciphering Cancer Stem Cell Self-Renewal Pathways.International journal of molecular and cellular medicine · 2025Review
- TTI-101 targets STAT3/c-Myc signaling pathway to suppress cervical cancer progression: an integrated experimental and computational analysis.Cancer cell international · 2024Article
- The Hippo pathway transcription factors YAP and TAZ play HPV-type dependent roles in cervical cancer.Nature communications · 2024Article
- STAT5 Is Necessary for the Metabolic Switch Induced by IL-2 in Cervical Cancer Cell Line SiHa.International journal of molecular sciences · 2024Article
- Selenadiazole-Induced Hela Cell Apoptosis through the Redox Oxygen Species-Mediated JAK2/STAT3 Signaling Pathway.ACS omega · 2024Article
- Cancer Mutations Converge on a Collection of Protein Assemblies to Predict Resistance to Replication Stress.Cancer discovery · 2024Article
- HPV E6/E7: insights into their regulatory role and mechanism in signaling pathways in HPV-associated tumor.Cancer gene therapy · 2024Review
- γ-Synuclein promotes proliferation and inhibits apoptosis of oral squamous cell carcinoma via JAK2/STAT5b signaling pathway.American journal of cancer research · 2024Article
- Review
- CREB1 activation promotes human papillomavirus oncogene expression and cervical cancer cell transformation.Journal of medical virology · 2023Article
- Exploitation of ATP-sensitive potassium ion (KOncogene · 2023Article
- SCCA1/SERPINB3 suppresses antitumor immunity and blunts therapy-induced T cell responses via STAT-dependent chemokine production.The Journal of clinical investigation · 2023Article
- Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Persistent infection with high-risk human papillomavirus (HPV) is the underlying cause of ~5% of all human cancers, including the majority of cervical carcinomas and many other ano-genital and oral cancers. A major challenge remains to identify key host targets of HPV and to reveal how they contribute to virus-mediated malignancy. The HPV E6 oncoprotein aberrantly activates the signal transducer and activator of transcription 3 (STAT3) transcription factor and this is achieved by a virus-driven increase in the levels of the pro-inflammatory cytokine interleukin-6 (IL-6) in HPV positive cervical cancers cells. Crucially, STAT3 activity is essential for the proliferation and survival of cervical cancer cells, suggesting that targeting STAT3 may have therapeutic potential. Unfortunately, the development of direct STAT3 inhibitors has been problematic in the clinic due to toxicity issues identified in early stage trials. To overcome this issue, we focused on the protein Janus kinase 2 (JAK2), which phosphorylates STAT3 and is essential for STAT3 activation. Here, we demonstrate that inhibiting JAK2 reduces cell proliferation and induces apoptosis in HPV transformed cervical cancer cells. We further establish that this is due to inhibition of phosphorylation of the JAK2 substrates STAT3 and STAT5. Finally, we demonstrate that the clinically available JAK2 inhibitor Ruxolitinib synergises with cisplatin in inducing apoptosis, highlighting JAK2 as a promising therapeutic target in HPV-driven cancers.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.