Next Article in Journal
Clinical Characteristics of Osimertinib Responder in Non-Small Cell Lung Cancer Patients with EGFR-T790M Mutation
Next Article in Special Issue
The Effects of Pertuzumab and Its Combination with Trastuzumab on HER2 Homodimerization and Phosphorylation
Previous Article in Journal
Triple Negative Breast Cancer Profile, from Gene to microRNA, in Relation to Ethnicity
Previous Article in Special Issue
Correction: Hiroshi Sugano et al. Nafamostat Mesilate Enhances the Radiosensitivity and Reduces the Radiation-Induced Invasive Ability of Colorectal Cancer Cells. Cancers 2018, 10, 386
Article Menu
Issue 3 (March) cover image

Export Article

Open AccessArticle
Cancers 2019, 11(3), 364;

Cucurbitacin D Reprograms Glucose Metabolic Network in Prostate Cancer

Department of Pharmaceutical Sciences, University of Tennessee Health Science Centre, Memphis, TN 38163, USA
Centre for Interdisciplinary Research in Basic Sciences, Jamia Millia Islamia, New Delhi 110025, India
Department South Dakota State University, Brookings, SD 57007, USA
Authors to whom correspondence should be addressed.
Received: 30 October 2018 / Revised: 25 February 2019 / Accepted: 8 March 2019 / Published: 14 March 2019
(This article belongs to the Collection Drug Resistance and Novel Therapies in Cancers)
Full-Text   |   PDF [14693 KB, uploaded 14 March 2019]   |  


Prostate cancer (PrCa) metastasis is the major cause of mortality and morbidity among men. Metastatic PrCa cells are typically adopted for aberrant glucose metabolism. Thus, chemophores that reprogram altered glucose metabolic machinery in cancer cells can be useful agent for the repression of PrCa metastasis. Herein, we report that cucurbitacin D (Cuc D) effectively inhibits glucose uptake and lactate production in metastatic PrCa cells via modulating glucose metabolism. This metabolic shift by Cuc D was correlated with decreased expression of GLUT1 by its direct binding as suggested by its proficient molecular docking (binding energy −8.5 kcal/mol). Cuc D treatment also altered the expression of key oncogenic proteins and miR-132 that are known to be involved in glucose metabolism. Cuc D (0.1 to 1 µM) treatment inhibited tumorigenic and metastatic potential of human PrCa cells via inducing apoptosis and cell cycle arrest in G2/M phase. Cuc D treatment also showed inhibition of tumor growth in PrCa xenograft mouse model with concomitant decrease in the expression of GLUT1, PCNA and restoration of miR-132. These results suggest that Cuc D is a novel modulator of glucose metabolism and could be a promising therapeutic modality for the attenuation of PrCa metastasis. View Full-Text
Keywords: cucurbitacin D; PrCa; miRNAs and glucose metabolism cucurbitacin D; PrCa; miRNAs and glucose metabolism

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

Share & Cite This Article

MDPI and ACS Style

Sikander, M.; Malik, S.; Chauhan, N.; Khan, P.; Kumari, S.; Kashyap, V.K.; Khan, S.; Ganju, A.; Halaweish, F.T.; Yallapu, M.M.; Jaggi, M.; Chauhan, S.C. Cucurbitacin D Reprograms Glucose Metabolic Network in Prostate Cancer. Cancers 2019, 11, 364.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Cancers EISSN 2072-6694 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top