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Review
. 2018 Mar;29(2):e32.
doi: 10.3802/jgo.2018.29.e32.

Chemoresistance in ovarian cancer: exploiting cancer stem cell metabolism

Affiliations
Review

Chemoresistance in ovarian cancer: exploiting cancer stem cell metabolism

Shan Shan Li et al. J Gynecol Oncol. 2018 Mar.

Abstract (VSports在线直播)

Ovarian cancer is most deadly gynecologic malignancies worldwide. Chemotherapy is the mainstay treatment for ovarian cancer. Despite the initial response is promising, frequent recurrence in patients with advanced diseases remains a therapeutic challenge. Thus, understanding the biology of chemoresistance is of great importance to overcome this challenge and will conceivably benefit the survival of ovarian cancer patients VSports手机版. Although mechanisms underlying the development of chemoresistance are still ambiguous, accumulating evidence has supported an integral role of cancer stem cells (CSCs) in recurrence following chemotherapy. Recently, tumor metabolism has gained interest as a reason of chemoresistance in tumors and chemotherapeutic drugs in combination with metabolism targeting approaches has been found promising in overcoming therapeutic resistance. In this review, we will summarize recent studies on CSCs and metabolism in ovarian cancer and discuss possible role of CSCs metabolism in chemoresistance. .

Keywords: Cancer Stem Cells; Drug Resistance, Neoplasm; Metabolism; Ovarian Neoplasms. V体育安卓版.

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Conflict of interest statement

No potential conflict of interest relevant to this article was reported.

Figures

Fig. 1
Fig. 1
Schematic representation of CSCs in ovarian cancer chemoresistance. Chemotherapeutics fail to eliminate CSCs which can regenerate the entire tumor and ultimately result in a relapse. Ovarian CSCs are resistant to chemotherapy due to several mechanisms including increased drug efflux, quiescence, enhanced DNA repair, autophagy, etc. ALDH, aldehyde dehydrogenase; CSC, cancer stem cell; EpCAM, epithelial cell adhesion molecule.
Fig. 2
Fig. 2
Schematic of key glycolysis and lipogenesis enzymes and inhibitors. 3PO, 3-(3-pyridinyl)-1-(4-pyridinyl)-2-propen-1-one; DIC, dicumarol; F-1,6-BP, fructose 1,6-bisphosphate; F6P, fructose-6-phosphate; FASN, fatty acid synthase; G6P, glucose-6-phosphate; HK2, hexokinase 2; LDH, lactate dehydrogenase; PDH, phosphate dehydrogenase; PDK1, 3-phosphoinositide-dependent protein kinase-1; PFK-1, phosphofructokinase-1.

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