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To identify therapeutic targetable fusion in uterine cervical cancer, for which no effective gene targeted therapy has yet been clinically applied, we analyzed RNA sequencing data from 306 cervical cancer samples. We detected 445 high confidence fusion transcripts and identified four samples that harbored <jats:italic>FGFR3-TACC3<\/jats:italic> fusion as an attractive therapeutic target. The frequency of <jats:italic>FGFR3-TACC3<\/jats:italic>-fusion-positive cervical cancer is also 1.9% (2\/103) in an independent cohort. Continuous expression of the <jats:italic>FGFR3-TACC3<\/jats:italic> fusion transcript and protein induced anchorage-independent growth in the cervical epithelial cell line established from the ectocervix (Ect1\/E6E7) but not in that from endocervix (End1\/E6E7). Injection of <jats:italic>FGFR3-TACC3<\/jats:italic> fusion-transfected-Ect1\/E6E7 cells subcutaneously into NOG mice generated squamous cell carcinoma xenograft tumors, suggesting the association between <jats:italic>FGFR3-TACC3<\/jats:italic> fusion and squamous cell carcinogenesis. Transfection of a <jats:italic>FGFR3-TACC3<\/jats:italic> fusion transcript into four cervical cancer cell lines (SiHa, ME180, HeLa, and Ca Ski) induced activation of the MAPK pathway and enhancement of cell proliferation. Transcriptome analysis of the <jats:italic>FGFR3-TACC3<\/jats:italic> fusion-transfected cell lines revealed that an <jats:italic>IL8<\/jats:italic>-triggered inflammatory response was increased, via activation of FGFR3\u2013MAPK signaling. Continuous expression of <jats:italic>FGFR3-TACC3<\/jats:italic> fusion led to activation of the PI3K\u2013AKT pathway only in the two cell lines that harbored <jats:italic>PIK3CA<\/jats:italic> mutations. Sensitivity to the <jats:italic>FGFR<\/jats:italic> inhibitor, BGJ398, was found to depend on <jats:italic>PIK3CA<\/jats:italic> mutation status. Dual inhibition of both FGFR and AKT showed an obvious synergistic effect in cell lines that harbor mutant <jats:italic>PIK3CA<\/jats:italic>. Additionally, TACC3 inhibitor, KHS101, suppressed FGFR3-TACC3 fusion protein expression and showed antitumor effect against <jats:italic>FGFR3-TACC3<\/jats:italic> fusion-transfected cell lines. <jats:italic>FGFR3-TACC3<\/jats:italic> fusion-positive cancer has frequent genetic alterations of the PI3K\/AKT pathway and selection of appropriate treatment based on PI3K\/AKT pathway status should be required.<\/jats:p>","DOI":"10.1038\/s41389-017-0018-2","type":"journal-article","created":{"date-parts":[[2018,1,22]],"date-time":"2018-01-22T08:29:18Z","timestamp":1516609758000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":48,"title":["Novel therapeutic strategy for cervical cancer harboring FGFR3-TACC3 fusions"],"prefix":"10.1038","volume":"7","author":[{"given":"Ryo","family":"Tamura","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2254-3378","authenticated-orcid":false,"given":"Kosuke","family":"Yoshihara","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tetsuya","family":"Saito","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ryosuke","family":"Ishimura","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Juan Emmanuel","family":"Mart\u00ednez-Ledesma","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hu","family":"Xin","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tatsuya","family":"Ishiguro","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yutaro","family":"Mori","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kaoru","family":"Yamawaki","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kazuaki","family":"Suda","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Seiya","family":"Sato","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hiroaki","family":"Itamochi","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Teiichi","family":"Motoyama","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yoichi","family":"Aoki","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7704-8104","authenticated-orcid":false,"given":"Shujiro","family":"Okuda","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Cristine R.","family":"Casingal","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hirofumi","family":"Nakaoka","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ituro","family":"Inoue","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Roel G. 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