Circ_0007331 knock‐down suppresses the progression of endometriosis via miR‐200c‐3p/HiF‐1α axis

Dong, Liang; Zhang, Lu; Liu, Hua; Xie, Meiting; Gao, Jing; Zhou, Xiaoyan; Zhao, Qinghong; Zhang, Silin; Yang, Jing

doi:10.1111/jcmm.15833

Cited by 25 publications

(16 citation statements)

References 32 publications

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“…Evidences have demonstrated aberrant circRNA expression in endometriosis [5,6]. Some studies showed that circRNAs promote the pathogenesis of endometriosis via miRNAs [7][8][9]. Our further work found that circ_0000673 was signi cantly deregulated in ectopic endomemtrium compared to eutopic endometrium [5].…”

Section: Introductionmentioning

confidence: 64%

“…Moreover, our ndings uncover that loss of circ_0000673 could promotes proliferation and migration of endometrial cells. Recent studies suggested that circATRNL1 promotes epithelial-mesenchymal transition(EMT) by regulating Yes-associated protein 1 [23], and high expression of circ_0007331 play a vital role in the proliferation and invasion in endometriosis [9]. The studies suggested the regulation effects of circRNAs in the progression of endometriosis.…”

Section: Discussionmentioning

confidence: 99%

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Downregulation of Circ_0000673 Promotes Cell Proliferation and Migration in Endometriosis Via Suppressing PTEN

Yang

Ban

Zhang

et al. 2021

Preprint

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Background: Endometriosis is a prevalent gynecologic disease, affecting up to 10% of women at reproductive age and approximately 50% of women with infertility. The function of circRNAs in various diseases has been highlighted. Dysregulated expression of circRNAs in endometriosis has been reported and circ_0000673 was significantly deregulated. However, its explicit role in pathogenesis of endometriosis is yet to be identified. Methods: circ_0000673 expression was detected in paried ectopic and eutopic endometrium using qPCR and fluorescent in situ hybridization. Knockdown of circ_0000673 in eutopic and normal endometrial stromal cells were done by transfection with lentivirus vectors. The proliferation activity of endometrial stromal cells was evaluated by CCK-8 assay and colony formation assay, while the migration capacity was valued by wound healing assay. PTEN, PI3K and p-AKT were detected by qPCR and western blotting. Dual luciferase assay was performed to assess the bonding between circ_0000673, PTEN and miR-616-3p.Results: The expression of circ_0000673 was reduced in ectopic endometrium. Knockdown of circ_0000673 significantly induced eutopic and normal endometrial cell proliferation and migration. Bioinformatic analysis predicted that circ_0000673 might sponge miR-616-3p. The effect of circ_0000673 knockdown could be recovered by miR-616-3p inhibitor and enhanced by miR-616-3p mimics. Meanwhile, qPCR and western blotting showed that circ_0000673 knockdown inhibited the expression of PTEN, and subsequently activated PI3K and p-Akt. Furthermore, PTEN was confirmed to be a target of miR-616-3p. Conclusion: The results demonstrated that deregulated expression of circ_0000673 could promote endometriosis progression via sponging miR-616-3p and further regulating PTEN.

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Section: Introductionmentioning

confidence: 64%

Section: Discussionmentioning

confidence: 99%

Downregulation of Circ_0000673 Promotes Cell Proliferation and Migration in Endometriosis Via Suppressing PTEN

Yang

Ban

Zhang

et al. 2021

Preprint

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show abstract

“…Our findings indicate that loss of circ_0000673 could promote the proliferation and migration of endometrial cells. Recent studies have suggested that circATRNL1 promotes the EMT by regulating Yes-associated protein 1 28 , and that high expression of circ_0007331 plays a vital role in the proliferation and invasion of cells in endometriosis 10 . These studies suggest that circRNAs play a regulatory role in the progression of endometriosis.…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies have found aberrant circRNA expression in endometriosis [6,7]. Some of these studies showed that circRNAs promote the pathogenesis of endometriosis via regulating the function of miRNAs [8][9][10]. In a previous work, we found that circ_0000673…”

Section: Introductionmentioning

confidence: 93%

“…Previous studies have found aberrant circRNA expression in endometriosis 6 , 7 . Some of these studies showed that circRNAs promote the pathogenesis of endometriosis via regulating the function of miRNAs 8 - 10 . In a previous work, we found that circ_0000673 in the ectopic endometrium (EC) was significantly downregulated compared to the eutopic endometrium (EU) 11 .…”

Section: Introductionmentioning

confidence: 99%

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Downregulation of circ_0000673 Promotes Cell Proliferation and Migration in Endometriosis via the Mir-616-3p/PTEN Axis

Yang¹,

Ban²,

Zhang³

et al. 2021

Int. J. Med. Sci.

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Endometriosis is a common gynecological disease, affecting up to 10% of women of reproductive age and approximately 50% of women with infertility. Circular RNAs (circRNAs) have been shown to be involved in a number of diseases. Dysregulated expression of circRNAs in endometriosis has been reported, and circ_0000673 was significantly downregulated. However, the details of its role in the pathogenesis of endometriosis are still poorly understood. We investigated the location and effects of the downregulation of circ_0000673 in endometriosis. We demonstrated that knockdown of circ_0000673 significantly increased the proliferation and migration of eutopic and normal endometrial cells. Bioinformatics analysis predicted that circ_0000673 might act as a sponge for miR-616-3p. We found that the effect of circ_0000673 knockdown could be recovered by miR-616-3p inhibitor and enhanced by miR-616-3p mimics. qPCR and western blot assays showed that circ_0000673 knockdown could decrease the expression of PTEN and increase the expression of PI3K and p-AKT. PTEN was confirmed to be a target of miR-616-3p. These results demonstrated that the downregulation of circ_0000673 could promote the progression of endometriosis by inactivating PTEN via the deregulation of miR-616-3p.

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Silencing of circ_0007299 suppresses proliferation, migration, and invasiveness and promotes apoptosis of ectopic endometrial stromal cells in endometriosis via miR-424-5p-dependent modulation of CREB1

Mao

Zhang

et al. 2022

Arch Gynecol Obstet

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Circ_0007331 knock‐down suppresses the progression of endometriosis via miR‐200c‐3p/HiF‐1α axis

Cited by 25 publications

References 32 publications

Downregulation of Circ_0000673 Promotes Cell Proliferation and Migration in Endometriosis Via Suppressing PTEN

Downregulation of Circ_0000673 Promotes Cell Proliferation and Migration in Endometriosis Via Suppressing PTEN

Downregulation of circ_0000673 Promotes Cell Proliferation and Migration in Endometriosis via the Mir-616-3p/PTEN Axis

Silencing of circ_0007299 suppresses proliferation, migration, and invasiveness and promotes apoptosis of ectopic endometrial stromal cells in endometriosis via miR-424-5p-dependent modulation of CREB1

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