Silencing the long noncoding RNA, TINCR, a molecular sponge of miR‑335, inhibits the malignant phenotype of epithelial ovarian cancer via FGF2 suppression
Authors: Yue Wang
Yuexun Xu
Xiaoli He
Yali Li
Rui Li
Journal: International Journal of Oncology (2019)
Discipline: CLINICAL MEDICINE
Keywords: Aberrant terminal differentiation-induced noncoding RNA (TINCR); epithelial ovarian cancer (EOC); tumor progression; microRNA-335 (miR-335); fibroblast growth factor 2 (FGF2)
Affiliations: Department of Obstetrics and Gynecology, Henan Province People's Hospital, The People's Hospital of Zhengzhou University, The People's Hospital of Henan University, Zhengzhou, Henan 450003, P.R. China.

Abstract:  Aberrant terminal differentiation‑induced noncoding RNA (TINCR) expression has been identified in multiple human cancer types and is functionally significant in cancer progression. However, to the best of our knowledge, no reported studies have investigated the expression pattern and precise role of TINCR in epithelial ovarian cancer (EOC). Here, TINCR expression levels in EOC tissues and cell lines were determined by reverse transcription‑quantitative polymerase chain reaction. Cell Counting Kit‑8 assays, flow cytometric analysis, Transwell migration and invasion assays, and in vivo xenograft experiments were performed to determine the influence of TINCR on the malignant phenotype of EOC cells in vitro and in vivo. The molecular mechanisms associated with the tumor‑promoting roles of TINCR during EOC progression were elucidated using a series of experiments. TINCR expression was higher in EOC tissues and cell lines compared with normal cells. An analysis of the association between TINCR expression and clinicopathological characteristics showed that increased TINCR expression was closely related to tumor size, FIGO stage, and lymphatic metastasis. In addition, the overall survival rates of EOC patients with high TINCR expression levels were lower than in those with low TINCR expression levels. Functional experiments showed that TINCR deficiency attenuated the proliferation, migration, and invasion of EOC cells in vitro and hindered EOC tumor growth in vivo. In addition, EOC cell apoptosis increased after TINCR knockdown. Mechanistically, TINCR was shown to function as a sponge of microRNA‑335 (miR‑335) in EOC cells, thereby regulating fibroblast growth factor 2 (FGF2) expression. miR‑335 inhibition partially counteracted the effect of TINCR knockdown on the aggressive behavior of EOC cells. This study showed, for the first time to the best of our knowledge, that silencing TINCR, which interacts with miR‑335, inhibited EOC progression in vitro and in vivo by decreasing FGF2 expression. Hence, this lncRNA could be a potential prognostic biomarker and effective target for therapeutic intervention in EOC. 

Retracted: No

PubPeer comments:
 Figs 2C, 4C, 6C. ![file] The brown box marks a panel that also appears in 2C, 5C, 6C of [Cheng et al (2020)] . ![file] ![file] The panel marked with a blue box appears in Cheng et al, but also in Figs 2D, 4D, 5D of [Yang et al (2019)] . ![] ![file] There may be matches with other panels, or with other papers in this oeuvre. https: docs.google.com spreadsheets d 1X401JM6CcpTSkbKsPsOl20pRKQ-ns1S_J5pTwtBjqPw edit#gid=0 , 
 *[left]* Fig 9A.  Representative images of tumor xenografts obtained from mice injected with si-TINCR- and si-NC-transfected EOC cells . *[right]* Fig 6A from [Sun et al (2020)] .  Representative images of tumor xenografts following subcutaneous injection of Y79 cells transfected with either si-SNHG14 or si-NC . ![file] Surprisingly similar. , 
 #1 Figs 2C, 4C, 6C again. Pink box added, to match a panel from Figs 2B, 4D of [Liu et al (2019)] . ![] ![] In context: ![] , 
 Retracted [22 August 2022] .  Following the publication of this paper, it was drawn to the Editors attention by a concerned reader that various panels showing the data from flow cytometry experiments in Figs. 2C, 4C and 6C, and certain of the tumor images featured in Fig. 9A, were strikingly similar to data appearing in different form in other articles by different authors. Owing to the fact that the contentious data in the above article had already been published elsewhere, or were already under consideration for publication, prior to its submission to *International Journal of Oncology*, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. ,