ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2014
The apoptotic effect of shikonin on human papillary thyroid carcinoma cells through mitochondrial pathway.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Shikonin Promotes Apoptosis and Attenuates Migration and Invasion of Human Esophageal Cancer Cells by Inhibiting Tumor Necrosis Factor Receptor-Associated Protein 1 Expression and AKT/mTOR Signaling Pathway.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Herbal Active Ingredients: An Emerging Potential for the Prevention and Treatment of Papillary Thyroid Carcinoma.BioMed research international · 2020Review
- Antiproliferative Effects of Alkaloid Evodiamine and Its Derivatives.International journal of molecular sciences · 2018Review
- Shikonin causes apoptosis by disrupting intracellular calcium homeostasis and mitochondrial function in human hepatoma cells.Experimental and therapeutic medicine · 2018Article
- Article
- Cbl-b-regulated extracellular signal-regulated kinase signaling is involved in the shikonin-induced apoptosis of lung cancer cellsExperimental and therapeutic medicine · 2015Article
- Inducing apoptosis effect of caffeic acid 3,4-dihydroxy-phenethyl ester on the breast cancer cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- Self-assembled supramolecular hetero-bimetallacycles for anticancer potency by intracellular release.Chemistry (Weinheim an der Bergstrasse, Germany) · 2014Article
- In vitro induction of erythrocyte phosphatidylserine translocation by the natural naphthoquinone shikonin.Toxins · 2014Article
- Altered antioxidant system stimulates dielectric barrier discharge plasma-induced cell death for solid tumor cell treatment.PloS one · 2014Article
- Shikonin induces apoptosis in the human gastric cancer cells HGC-27 through mitochondria-mediated pathway.Pharmacognosy magazineArticle
Corrections and comments
- Retraction · 2017-04-20Compromised Peer Review · Investigation by Journal/Publisher · · Journal published by SAGE starting in 2017
- Retracted
Authors and funding
4 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study aims to explore the apoptotic function of shikonin on the papillary thyroid cancer cells and the related mechanism. The papillary thyroid cancer cell lines K1 and W3 and thyroid follicular epithelial cells NTHY-ORI 3-1 were treated with different concentrations of shikonin. Cell proliferation was tested. Morphological changes of the apoptotic cells were observed by Hoechst 33342 staining. The apoptosis rate of the papillary thyroid cancer cells was measured with flow cytometry. Changes of the cell cycle were explored. The mitochondrial membrane potential changes were analyzed after JC-1 staining. Bcl-2 family proteins and caspase-3 expression with shikonin treatment was analyzed by real-time fluorescence polymerase chain reaction (PCR). Cell proliferation of K1 and W3 was inhibited by shikonin, and the inhibition was dose-time dependent. Papillary thyroid carcinoma cells treated by shikonin had no obvious cell cycle arrest but were observed with the higher apoptosis rate and the typical apoptotic morphological changes of the cell nucleus. JC-1 staining showed that shikonin reduced the mitochondrial membrane potential of papillary thyroid carcinoma cells. Real-time PCR results showed that shikonin significantly increased Bax and caspase-3 expression and upregulated Bcl-2 expression in a dose-dependent manner in papillary thyroid carcinoma cells. However, the NTHY-ORI 3-1 was almost not affected by shikonin treatment. Shikonin can inhibit K1 and W3 cell proliferation in a dose- and time-dependent manner, enhance Bax levels, reduce anti-apoptotic protein Bcl-2 levels, result in decreasing mitochondrial membrane potential and activating caspase-3 enzyme, and finally lead to apoptosis.
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Registered trials
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