{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,20]],"date-time":"2026-05-20T20:46:03Z","timestamp":1779309963654,"version":"3.51.4"},"reference-count":25,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2013,11,12]],"date-time":"2013-11-12T00:00:00Z","timestamp":1384214400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cancer Science"],"published-print":{"date-parts":[[2013,12]]},"abstract":"<jats:p>Cancer cells require glucose to support their rapid growth through a process known as aerobic glycolysis, or the <jats:styled-content style=\"fixed-case\">W<\/jats:styled-content>arburg effect. As in ovarian cancer cells, increased metabolic activity and glucose concentration has been linked to aggressiveness of cancer. However, it is unclear as to whether targeting the glycolytic pathway may kill the malignant cells and likely have broad therapeutic implications against ovarian cancer metastasis. In the present research, we found that <jats:styled-content style=\"fixed-case\">EF<\/jats:styled-content>24, a <jats:styled-content style=\"fixed-case\">HIF<\/jats:styled-content>\u20101\u03b1 inhibitor, could significantly block glucose uptake, the rate of glycolysis, and lactate production compared with vehicle treatment in <jats:styled-content style=\"fixed-case\">SKOV<\/jats:styled-content>\u20103, <jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>2780 and <jats:styled-content style=\"fixed-case\">OVCAR<\/jats:styled-content>\u20103 cells. These results might possibly contribute to the further observation that <jats:styled-content style=\"fixed-case\">EF<\/jats:styled-content>24 could inhibit ovarian cancer cell migration and invasion from wound healing and Transwell assays. Furthermore, as an important mediator of glucose metabolism, glucose transporter\u00a01 (<jats:styled-content style=\"fixed-case\">G<\/jats:styled-content>lut1) was found to contribute to the function of <jats:styled-content style=\"fixed-case\">EF<\/jats:styled-content>24 in both energy metabolism and metastasis. To examine the effect of <jats:styled-content style=\"fixed-case\">EF<\/jats:styled-content>24 and the mediated role of <jats:styled-content style=\"fixed-case\">G<\/jats:styled-content>lut1 <jats:italic>in\u00a0vivo<\/jats:italic> in a xenograph subcutaneous tumor model, intraperitoneal metastasis and lung metastasis model were introduced. Our results indicated that <jats:styled-content style=\"fixed-case\">EF<\/jats:styled-content>24 treatment could inhibit tumor growth, intraperitoneal metastasis and lung metastasis of <jats:styled-content style=\"fixed-case\">SKOV<\/jats:styled-content>\u20103 cells, and <jats:styled-content style=\"fixed-case\">G<\/jats:styled-content>lut1 is a possible mediator for the role of <jats:styled-content style=\"fixed-case\">EF<\/jats:styled-content>24. In conclusion, our results highlight that an anti\u2010cancer reagent with an inhibiting effect on energy metabolism could inhibit metastasis, and <jats:styled-content style=\"fixed-case\">EF<\/jats:styled-content>24 is a possible candidate for anti\u2010metastasis therapeutic applications for ovarian cancer.<\/jats:p>","DOI":"10.1111\/cas.12293","type":"journal-article","created":{"date-parts":[[2013,10,12]],"date-time":"2013-10-12T01:34:49Z","timestamp":1381541689000},"page":"1690-1696","source":"Crossref","is-referenced-by-count":34,"title":["Therapeutic role of <scp>EF<\/scp>24 targeting glucose transporter 1\u2010mediated metabolism and metastasis in ovarian cancer cells"],"prefix":"10.1111","volume":"104","author":[{"given":"Dandan","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Obstetrics and Gynecology First Affiliated Hospital of Harbin Medical University Harbin Heilongjiang 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