Withdrawal: “Long Non‐coding RNA NEAT1 Drives the Development of Polycystic Ovary Syndrome via Sponging Multiple MicroRNAs” by Xia Sang and Yuzhen Zhang

Sang, Xia; Zhang, Yuzhen

doi:10.1002/cbin.11349

Cited by 5 publications

(8 citation statements)

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“…The initial finding from our research showed that NEAT1 and IGF1 were highly expressed while miR-381 was lowly expressed in PCOS. In line with the results in our study, a recent study highlighted that NEAT1 expression tended to upregulate in PCOS [9]. Similarly, NEAT1 was upregulated in tissues and cells of PCOS [9].…”

Section: Discussionsupporting

confidence: 92%

“…Of the lncRNA family, nuclear-enriched abundant transcript 1 (NEAT1) has been revealed to regulate ovarian carcinogenesis and act as a potential biomarker for antineoplastic therapies [7,8]. Moreover, NEAT1 has the ability to promote ovarian granulosa cell proliferation and suppress apoptosis through acting as a sponge of microRNAs (miRNAs) [9]. miRNAs that are differentially expressed in PCOS are related to the pathophysiology of the disease [10].…”

Section: Introductionmentioning

confidence: 99%

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RETRACTED ARTICLE: Downregulating lncRNA NEAT1 induces proliferation and represses apoptosis of ovarian granulosa cells in polycystic ovary syndrome via microRNA-381/IGF1 axis

Zhen

Li²,

et al. 2021

J Biomed Sci

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Objective Researchers have revealed the combined functions of long noncoding RNAs (lncRNAs) and microRNA (miRNAs) in polycystic ovary syndrome (PCOS). This study aimed to understand the role of nuclear-enriched abundant transcript 1 (NEAT1) and miR-381 involving insulin-like growth factor 1 (IGF1) in PCOS. Methods PCOS rat model was established by dehydroepiandrosterone induction. NEAT1, miR-381 and IGF1 expression in ovarian granulosa cells of PCOS patients and ovarian tissues of PCOS rats were tested. Bioinformatics website and dual luciferase reporter gene assay were utilized to verify the relationship between NEAT1 and miR-381 and that between miR-381 and IGF1. Levels of sex hormone, pathological changes and ovarian granulosa cell apoptosis in ovarian tissues of PCOS rats were detected. Ovarian granulosa cell proliferation and apoptosis were analyzed in vitro. Results NEAT1 and IGF1 expression increased while miR-381 expression decreased in the ovarian granulosa cells of patients with PCOS and the ovarian tissues of PCOS rats. In in vivo experiments, interference with NEAT1 improved the levels of sex hormones, alleviated pathological changes and suppressed ovarian granulosa cell apoptosis in the ovarian tissues of PCOS rats. In in vitro cell experiments, interference with NEAT1 suppressed apoptosis and enhanced cell proliferation of ovarian granulosa cells. NEAT1 interference-mediated effect would be reversed by up-regulating miR-381. NEAT1 acted as a ceRNA to adsorb miR-381 to target IGF1. Overexpression of IGF1 reversed the inhibitory effect of miR-381 on ovarian granulosa cell apoptosis. Conclusion Interference with NEAT1 increases miR-381 and reduces IGF1 levels, effectively improving the levels of sex hormones and reducing the pathological damage of ovarian tissue in rats with PCOS.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: Downregulating lncRNA NEAT1 induces proliferation and represses apoptosis of ovarian granulosa cells in polycystic ovary syndrome via microRNA-381/IGF1 axis

Zhen

Li²,

et al. 2021

J Biomed Sci

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“…***p < 0.001, **p < 0.01, and *p < 0.05 we identified miR-483 as a target of NEAT1, and the exogenous expression of NEAT1 reduced miR-483 expression, subsequently upregulating the expression of N-cadherin, Vimentin and Snail and promoting the EMT in osteosarcoma cells. Our results further confirmed the sponging of miR-483 by NEAT1, which has also been reported by Xia Sang in ovarian granulosa cells [48]. Using this mechanism, NEAT1 finely restrains the expression of miR-483 and promotes the proliferation and migration of osteosarcoma cells.…”

Section: Discussionsupporting

confidence: 90%

“…In summary, these three components constituted a network that regulates the EMT of osteosarcoma cells. Although our study is not the first study reporting the association between NEAT1 and miR-483 [48], it describes the regulation of STAT3 by miR-483 and their functions in regulating the EMT and metastasis of osteosarcoma cells for the first time. Our findings are also consistent with previous reports that overexpression of NEAT1 increases the proliferation, invasion and metastasis of oesophageal squamous cell carcinoma [49], while NEAT1 knockdown impairs cell invasion and migration and reduces the levels of EMTassociated proteins in renal cell carcinoma [50].…”

Section: Discussionmentioning

confidence: 92%

The lncRNA NEAT1 promotes the epithelial-mesenchymal transition and metastasis of osteosarcoma cells by sponging miR-483 to upregulate STAT3 expression

Xiao

et al. 2021

Cancer Cell Int

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Background Osteosarcoma is one of the most prevalent primary bone tumours in adolescents. Accumulating evidence shows that aberrant expression of the long non-coding RNA (lncRNA) NEAT1 and microRNA-483 (miR-483) contribute to the epithelial-mesenchymal transition (EMT), invasion and metastasis of tumour cells. However, the potential regulatory effects of NEAT1 and miR-483 on the EMT of osteosarcoma remain elusive. Methods The expression of the NEAT1, miR-483, signal transducer and activator of transcription-1 (STAT1), STAT3, and EMT-associated markers was measured using qRT-PCR or western blotting. NEAT1 overexpression or knockdown was induced by lentivirus-mediated transfection. A luciferase reporter assay was employed to confirm the association between NEAT1/miR-483 and miR-483/STAT3. RNA immunoprecipitation (RIP) was also performed to verify the NEAT1 and miR-483 interaction. Wound healing and transwell assays were implemented to assess the migration and invasion of U2OS cells. Unilateral subcutaneous injection of U2OS into nude mice was performed to investigate tumour metastasis in vivo. Results The expression of miR-483 was downregulated in both osteosarcoma cell lines and osteosarcoma tissues. The overexpression of miR-483 suppressed the migration, invasion, and expression of EMT-associated proteins in U2OS cells, while simultaneous overexpression of STAT3 partially relieved this suppression. Mechanistically, miR-483 specifically targeted the 3′ untranslated region (3′UTR) of STAT3 and repressed its expression. However, NEAT1 sponged miR-438, increased STAT3 expression, and repressed STAT1 expression, subsequently increasing the EMT of osteosarcoma cells. The knockdown of NEAT1 in transplanted U2OS cells impaired the liver and lung metastases of osteosarcoma in nude mice. Moreover, NEAT1 silencing inhibited the mesenchymal- epithelial transition (MET) of osteosarcoma at metastasis sites. Conclusions The lncRNA NEAT1/miR-483/STAT3 axis plays a crucial role in regulating the metastasis of osteosarcoma and potentially represents one appealing therapeutic target for osteosarcoma treatment in the future.

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“…LncRNA ZFAS1 combining with miR-129 prevents miRNA-mediated degradation of HMGB1, inhibiting the proliferation activity while promoting the apoptosis of GCs (48). The expression of NEAT1 is upregulated in PCOS ovarian tissue, promoting the proliferation of human granulosa-like tumor cell line KGN via several miRNAs (i.e., miR-16, miR-483 and miR-324-3p) (47). However, whether the upregulated NEAT1 causes corpus luteum dysfunction in PCOS, like NEAT1 KO mice (38), is unclear.…”

Section: Cell Proliferation And/or Apoptosismentioning

confidence: 99%

Long non-coding RNAs: novel players in the pathogenesis of polycystic ovary syndrome

et al. 2021

Ann Transl Med

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Long non-coding RNAs (lncRNAs) are a class of transcripts (>200 nucleotides) lacking proteincoding capacity. Based on the complex three-dimensional structure, lncRNAs are involved in many biological processes and can regulate the expression of target genes at chromatin modification, transcriptional and post-transcriptional levels. LncRNAs have been studied in multiple diseases but little is known about their role(s) in polycystic ovary syndrome (PCOS), the most common endocrinological disorder in reproductiveaged women around the world. In this review, we characterized and explored the potential mechanisms of lncRNAs in the pathogenesis of PCOS. We found that lncRNAs play a molecular role in PCOS mainly by functioning as the competitive endogenous RNA (ceRNA) and are significantly correlated with some clinical phenotypes. We summarized in detail regarding aberrant lncRNAs in different specimens of women with PCOS [i.e., granulosa cells (GCs), cumulus cells (CCs), follicular fluid (FF), peripheral blood] and various PCOS rodent models [i.e., dehydroepiandrosterone (DHEA) and letrozole induced models]. In clinical practice, detection of lncRNAs in serum might enable early diagnosis. Furthermore, new lncRNAbased classifications might be emerging as potent predictors of a particular phenotype in PCOS. Overall, we proposed new insights for the application of precision medicine approaches to the management of PCOS.

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Withdrawal: “Long Non‐coding RNA NEAT1 Drives the Development of Polycystic Ovary Syndrome via Sponging Multiple MicroRNAs” by Xia Sang and Yuzhen Zhang

Abstract: Schenkmann, and John Wiley & Sons Ltd. on behalf of the International Federation for Cell Biology. The withdrawal has been agreed because the authors could not be reached for fi nal approval of the publication of the article.

Cited by 5 publications

References 0 publications

RETRACTED ARTICLE: Downregulating lncRNA NEAT1 induces proliferation and represses apoptosis of ovarian granulosa cells in polycystic ovary syndrome via microRNA-381/IGF1 axis

RETRACTED ARTICLE: Downregulating lncRNA NEAT1 induces proliferation and represses apoptosis of ovarian granulosa cells in polycystic ovary syndrome via microRNA-381/IGF1 axis

The lncRNA NEAT1 promotes the epithelial-mesenchymal transition and metastasis of osteosarcoma cells by sponging miR-483 to upregulate STAT3 expression

Long non-coding RNAs: novel players in the pathogenesis of polycystic ovary syndrome

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