Journal
INTERNATIONAL JOURNAL OF GYNECOLOGICAL CANCER
Volume 27, Issue 4, Pages 634-642Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/IGC.0000000000000951
Keywords
Cervical cancer; D-dopachrome tautomerase; Macrophage migration inhibitory factor
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Funding
- National Natural Science Foundation of China [81502230]
- Shanghai Municipal Commission of Health and Family Planning [20154Y0010, 20164Y0190]
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Objective D-dopachrome tautomerase (D-DT) is a homologue of macrophage migration inhibitory factor (MIF) with similar functions. However, the possible biological roles of D-DT in cervical cancer remain unknown so far. Methods D-dopachrome tautomerase was assessed by immunohistochemistry in 83 cervical cancer and 31 normal cervix tissues. The stable knockdown of D-DT and MIF by lentivirus-delivered short hairpin RNA was established, and tumor growth was examined in vitro and in vivo. The effects of D-DT and MIF on the migration and invasion were further detected by wound healing assay and transwell assay. Western blot was used to explore the mechanism of D-DT and MIF in cervical cancer pathogenesis. Results We found that D-DT was significantly high in cervical cancer, which correlated with lymph node metastasis. The knockdown of D-DT and MIF, individually and additively, inhibited the proliferation, migration, and invasion in HeLa and SiHa cells and restrained the growth of xenograft tumor. The ablation of D-DT and MIF rescued the expression of E-cadherin and inhibited the expression of PCNA, cyclin D1, gankyrin, Sam68, and vimentin, as well as phospho-Akt and phospho-glycogen synthase kinase 3-. Conclusions The inhibition of D-DT and MIF in combination may represent a potential therapeutic strategy for cervical cancer.
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