ArticleCell death & disease2018
Plumbagin inhibits the proliferation and survival of esophageal cancer cells by blocking STAT3-PLK1-AKT signaling.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 119 citations in OpenAlex.
- PEG-GE11-modified nanoplatform for co-delivery of cisplatin and plumbagin in targeted therapy of oral squamous cell carcinoma.RSC advances · 2026Article
- A Derivative of Plumbagin Targets the JAK2/STAT3 Pathway to Inhibit the Progression of Oral Squamous Cell Carcinoma.Molecules (Basel, Switzerland) · 2026Article
- Exploring the Therapeutic Potential of Plumbagin: Its Current Applications in Cancer and Neuropsychiatric Disorders.Current medicinal chemistry · 2026Review
- Lipocalin-2 drives brain metastatic progression through reciprocal tumor-microenvironment interactions in lung cancer.Signal transduction and targeted therapy · 2025Article
- The Occurrence, Uses, Biosynthetic Pathway, and Biotechnological Production of Plumbagin, a Potent Antitumor Naphthoquinone.Molecules (Basel, Switzerland) · 2025Review
- Article
- PSMD12 promotes hepatocellular carcinoma progression by stabilizing CDK1.Frontiers in immunology · 2025Article
- The phytochemical plumbagin: mechanism behind its "pleiotropic" nature and potential as an anticancer treatment.Archives of toxicology · 2024Review
- Pharmacological Features and Therapeutic Implications of Plumbagin in Cancer and Metabolic Disorders: A Narrative Review.Nutrients · 2024Review
- Erianin Impedes the Proliferation and Metastatic Migration Through Suppression of STAT-3 Phosphorylation in Human Esophageal Cancer Cells.Applied biochemistry and biotechnology · 2024Article
- Plumbagin induces ferroptosis in colon cancer cells by regulating p53-related SLC7A11 expression.Heliyon · 2024Article
- Interactions of plumbagin with five common antibiotics against Staphylococcus aureus in vitro.PloS one · 2024Article
- Article
- GATA6-AS1 via Sponging miR-543 to Regulate PTEN/AKT Signaling Axis Suppresses Cell Proliferation and Migration in Gastric Cancer.Mediators of inflammation · 2023Article
- Unraveling the Complexity of Regulated Cell Death in Esophageal Cancer: from Underlying Mechanisms to Targeted Therapeutics.International journal of biological sciences · 2023Review
- HN1L/AP-2γ/PLK1 signaling drives tumor progression and chemotherapy resistance in esophageal squamous cell carcinoma.Cell death & disease · 2022Article
- Molecular mechanism, regulation, and therapeutic targeting of the STAT3 signaling pathway in esophageal cancer (Review).International journal of oncology · 2022Article
- Comprehensive Analysis and Experimental Validation of a Novel Estrogen/Progesterone-Related Prognostic Signature for Endometrial Cancer.Journal of personalized medicine · 2022Article
- Pharmacogenomics of in vitro response of the NCI-60 cancer cell line panel to Indian natural products.BMC cancer · 2022Article
- Role of Plant-Derived Active Constituents in Cancer Treatment and Their Mechanisms of Action.Cells · 2022Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Esophageal squamous cell carcinoma (ESCC) is one of the deadliest cancers, and it requires novel treatment approaches and effective drugs. In the present study, we found that treatment with plumbagin, a natural compound, reduced proliferation and survival of the KYSE150 and KYSE450 ESCC cell lines in a dose-dependent manner in vitro. The drug also effectively inhibited the viability of primary ESCC cells from fresh biopsy specimens. Furthermore, plumbagin-induced mitotic arrest and massive apoptosis in ESCC cells. Notably, the drug significantly suppressed the colony formation capacity of ESCC cells in vitro and the growth of KYSE150 xenograft tumors in vivo. At the molecular level, we found that exposure to plumbagin decreased both polo-like kinase 1 (PLK1) and phosphorylated protein kinase B (p-AKT) expression in both ESCC cell lines. Enforced PLK1 expression in ESCC cells not only markedly rescued cells from plumbagin-induced apoptosis and proliferation inhibition but also restored the impaired AKT activity. Furthermore, signal transducer and activator of transcription 3 (STAT3), a transcription factor of PLK1, was also inactivated in plumbagin-treated ESCC cells; however, the overexpression of a constitutively activated STAT3 mutant, STAT3C, reinstated the plumbagin-elicited blockade of PLK1-AKT signaling in ESCC cells. Taken together, these findings indicate that plumbagin inhibits proliferation and potentiates apoptosis in human ESCC cells in vitro and in vivo. Plumbagin may exert these antitumor effects by abrogating STAT3-PLK1-AKT signaling, which suggests that plumbagin may be a novel, promising anticancer agent for the treatment of ESCC.
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