Asset Details
Do you wish to reserve the book?
Shikonin Inhibits Tumor Growth in Mice by Suppressing Pyruvate Kinase M2-mediated Aerobic Glycolysis
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Shikonin Inhibits Tumor Growth in Mice by Suppressing Pyruvate Kinase M2-mediated Aerobic Glycolysis
Do you wish to request the book?
Shikonin Inhibits Tumor Growth in Mice by Suppressing Pyruvate Kinase M2-mediated Aerobic Glycolysis
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Shikonin Inhibits Tumor Growth in Mice by Suppressing Pyruvate Kinase M2-mediated Aerobic Glycolysis
2018
Overview
Shift metabolism profile from mitochondrial oxidative phosphorylation to aerobic glycolysis (Warburg effect) is a key for tumor cell growth and metastasis. Therefore, suppressing the tumor aerobic glycolysis shows a great promise in anti-tumor therapy. In the present study, we study the role of shikonin, a naphthoquinone isolated from the traditional Chinese medicine Lithospermum, in inhibiting tumor aerobic glycolysis and thus tumor growth. We found that shikonin dose-dependently inhibited glucose uptake and lactate production in Lewis lung carcinoma (LLC) and B16 melanoma cells, confirming the inhibitory effect of shikonin on tumor aerobic glycolysis. Treatment of shikonin also decreased tumor cell ATP production. Furthermore, pyruvate kinase M2 (PKM2) inhibitor or activator respectively altered the effect of shikonin on tumor cell aerobic glycolysis, suggesting that suppression of cell aerobic glycolysis by shikonin is through decreasing PKM2 activity. Western blot analysis confirmed that shikonin treatment reduced tumor cell PKM2 phosphorylation though did not reduce total cellular PKM2 level.
In vitro
assay also showed that shikonin treatment significantly promoted tumor cell apoptosis compared to untreated control cells. Finally, when mice implanted with B16 cells were administered with shikonin or control vehicle, only shikonin treatment significantly decreased B16 tumor cell growth. In conclusion, this study demonstrates that shikonin inhibits tumor growth in mice by suppressing PKM2-mediated aerobic glycolysis.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ 14/63
/ 64/60
/ 96/2
/ 96/31
/ Adenosine Triphosphate - metabolism
/ Animals
/ Antineoplastic Agents, Phytogenic - pharmacology
/ Antineoplastic Agents, Phytogenic - therapeutic use
/ Drug Screening Assays, Antitumor
/ Drugs, Chinese Herbal - pharmacology
/ Drugs, Chinese Herbal - therapeutic use
/ Enzyme Inhibitors - pharmacology
/ Humanities and Social Sciences
/ Male
/ Melanoma
/ Melanoma, Experimental - drug therapy
/ Mice
/ Naphthoquinones - pharmacology
/ Naphthoquinones - therapeutic use
/ Neoplasm Proteins - antagonists & inhibitors
/ Phosphorylation - drug effects
/ Protein Processing, Post-Translational - drug effects
/ Pyruvate Kinase - antagonists & inhibitors
/ Science
/ Shikonin
/ Stomach Neoplasms - pathology
/ Traditional Chinese medicine
/ Tumors
