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dc.contributor.authorChoi, Pui-Wah
dc.contributor.authorSo, Wai Wing
dc.contributor.authorYang, Junzheng
dc.contributor.authorLiu, Shubai
dc.contributor.authorTong, Ka Kui
dc.contributor.authorKwan, Kin Ming
dc.contributor.authorKwok, Jamie S-L
dc.contributor.authorTsui, Stephen KW
dc.contributor.authorNg, Shu-Kay
dc.contributor.authorHales, Karen H
dc.contributor.authorHales, Dale B
dc.contributor.authorWelch, William R
dc.contributor.authorCrum, Christopher P
dc.contributor.authorFong, Wing-Ping
dc.contributor.authorBerkowitz, Ross S
dc.contributor.authorNg, Shu-Wing
dc.description.abstractEpidemiologic and histopathologic findings and the laying hen model support the long-standing incessant ovulation hypothesis and cortical inclusion cyst involvement in sporadic ovarian cancer development. MicroRNA-200 (miR-200) family is highly expressed in ovarian cancer. Herewith, we show that ovarian surface epithelial (OSE) cells with ectopic miR-200 expression formed stabilized cysts in three-dimensional (3D) organotypic culture with E-cadherin fragment expression and steroid hormone pathway activation, whereas ovarian cancer 3D cultures with miR-200 knockdown showed elevated TGF-β expression, mitotic spindle disorientation, increased lumenization, disruption of ROCK-mediated myosin II phosphorylation, and SRC signaling, which led to histotype-dependent loss of collective movement in tumor spread. Gene expression profiling revealed that epithelial–mesenchymal transition and hypoxia were the top enriched gene sets regulated by miR-200 in both OSE and ovarian cancer cells. The molecular changes uncovered by the in vitro studies were verified in both human and laying hen ovarian cysts and tumor specimens. As miR-200 is also essential for ovulation, our results of estrogen pathway activation in miR-200-expressing OSE cells add another intriguing link between incessant ovulation and ovarian carcinogenesis.
dc.publisherNature Publishing Group
dc.subject.fieldofresearchClinical Sciences
dc.subject.fieldofresearchOncology and Carcinogenesis
dc.subject.keywordsScience & Technology
dc.subject.keywordsLife Sciences & Biomedicine
dc.subject.keywordsBiochemistry & Molecular Biology
dc.subject.keywordsCell Biology
dc.titleMicroRNA-200 family governs ovarian inclusion cyst formation and mode of ovarian cancer spread
dc.typeJournal article
dc.type.descriptionC1 - Articles
dcterms.bibliographicCitationChoi, P-W; So, WW; Yang, J; Liu, S; Tong, KK; Kwan, KM; Kwok, JS-L; Tsui, SKW; Ng, S-K; Hales, KH; Hales, DB; Welch, WR; Crum, CP; Fong, W-P; Berkowitz, RS; Ng, S-W, MicroRNA-200 family governs ovarian inclusion cyst formation and mode of ovarian cancer spread, Oncogene, 2020, 39 (20), pp. 4045-4060
gro.hasfulltextNo Full Text
gro.griffith.authorNg, Shu Kay Angus

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