Circular RNA MTO1 Inhibits the Proliferation and Invasion of Ovarian Cancer Cells Through the miR-182-5p/KLF15 Axis

Wang, Ning; Cao, Qin-Xue; Tian, Jie; Ren, Luping; Cheng, Hongyan; Yang, Shao-Qin

doi:10.1177/0963689720943613

Cited by 22 publications

(9 citation statements)

References 41 publications

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“…15 Also, circMTO1 was considered as a biomarker for OC, which could suppress OC proliferation and invasion via regulating miR-182-5p/KLF15. 16 Hence, elucidating the role of circRNA in cancers can provide us with a deeper understanding of the tumorigenesis mechanism, thus providing a new direction for cancer treatment.…”

Section: Introductionmentioning

confidence: 99%

Hsa_circ_0015326 Promotes the Proliferation, Invasion and Migration of Ovarian Cancer Through miR-127-3p/MYB

Zhang¹,

Liu²,

Li³

et al. 2021

CMAR

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Background More and more evidences show that circular RNA (circRNA) has an important role in ovarian cancer (OC). Hsa_circ_0015326 is a newly discovered upregulated circRNA in OC, but its role and mechanism in OC have not been studied yet. Methods Quantitative real-time PCR was used to detect the expression of hsa_circ_0015326, microRNA (miR)-127-3p and MYB. The viability, colony number, cell cycle process, invasion, migration and apoptosis of cells were determined using cell counting kit 8 assay, colony formation assay, flow cytometry, transwell assay and wound healing assay. Moreover, the protein expression levels of metastasis, proliferation, apoptosis markers and MYB were assessed using Western blot analysis. The interaction between miR-127-3p and hsa_circ_0015326 or MYB was confirmed by dual-luciferase reporter assay and RNA immunoprecipitation assay. Xenograft tumors were built to explore the role of hsa_circ_0015326 in OC tumor growth in vivo. Results Elevated expression of hsa_circ_0015326 was identified in OC tissues and cells. Loss-of-function experiments suggested that silenced hsa_circ_0015326 inhibited the proliferation, invasion, migration, and promoted the apoptosis of OC cells in vitro, as well as inhibited OC tumorigenesis in vivo. Mechanically, hsa_circ_0015326 sponged miR-127-3p and miR-127-3p targeted MYB. The rescue experiments revealed that miR-127-3p inhibitor reversed the inhibitory effect of hsa_circ_0015326 silencing on OC progression, and MYB overexpression reversed the suppressive effect of miR-127-3p on OC progression. In addition, our data indicated that MYB expression was positively regulated by hsa_circ_0015326. Conclusion This study showed that hsa_circ_0015326 could facilitate OC progression by regulating the miR-127-3p/MYB axis, which suggested that it might become a potential target for the treatment of OC.

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Section: Introductionmentioning

confidence: 99%

Hsa_circ_0015326 Promotes the Proliferation, Invasion and Migration of Ovarian Cancer Through miR-127-3p/MYB

Zhang¹,

Liu²,

Li³

et al. 2021

CMAR

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“…13 Circ-MTO1 suppresses ovarian cancer cell progression and metastasis by sponging miR-182-5p and upregulating KLF15 expression. 14 In the present study, miR-510-5p was identified as a target for circ-ELF2 among seven candidate miRNAs. MiR-510-5p was previously identified as a tumor-suppressive miRNA in several human malignancies, such as renal cell carcinoma.…”

Section: Discussionmentioning

confidence: 58%

<p>Circ-ELF2 Acts as a Competing Endogenous RNA to Facilitate Glioma Cell Proliferation and Aggressiveness by Targeting MiR-510-5p/MUC15 Signaling</p>

Zhang¹,

Xu²,

Guo³

et al. 2020

OTT

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Objective: Glioma (GM) is a common type of malignant and aggressive tumor in brain with poor prognosis. Circular RNAs (circRNAs) are well-known regulators in cancer progression. However, its molecular basis in GM remains to be investigated. Materials and Methods: CircRNA microarray was used to detect differentially expressed circRNAs in GM and matched noncancerous tissues. qRT-PCR was applied to detect the expression profile of circ-ELF2 in GM tissue specimens and cell lines. CCK-8, clone formation, AO/EB staining, flow cytometry, wound healing, and transwell assays were performed to identify the functions of circ-ELF2 in GM cells. The distribution of circ-ELF2 was analyzed by RNA-FISH and subcellular fractionation assay. Dual-luciferase reporter assay was applied to verify the predicted binding sites between miR-510-5p and circ-ELF2/MUC15 3ʹ-UTR. Rescue assay was finally conducted to explore whether the oncogenic role of circ-ELF2 was partially attributed to miR-510-5p/MUC15 signaling. Results: We observed that circ-ELF2 was significantly upregulated in GM tissues, which was analyzed by circRNA microarray and qRT-PCR. Upregulation of circ-ELF2 was associated with poor prognosis and high recurrence rate for GM patients after surgery. The collapse of circ-ELF2 caused growth arrest and downregulation of cell migratory and invasive potential of GM cells and promoted cell apoptosis. In contrast, elevated expression of circ-ELF2 led to the opposite effect. Mechanistically, circ-ELF2 acted as a competing endogenous RNA (ceRNA) for miR-510-5p to positive modulate MUC15 expression at posttranscriptional level. Circ-ELF2 upregulated MUC15 by sponging miR-510-5p, thus promoting GM growth and aggressiveness. Conclusion: This study indicates that circ-ELF2/miR-510-5p/MUC15 signaling plays a key role in promoting the occurrence and development of GM.

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“…Further optimization of benzimidazole turns out a dimeric benzimidazole and bisbenzimide compound, targaprimir-96, which shows a favorable pharmacokinetics profile and is effective at releasing tumor burden in a triple-negative breast cancer xenograft mouse model [65]. Another dimeric benzimidazole and bisbenzimide analog, targaprimir (TGP)-515, is UBAP2 promotes proliferation and inhibits apoptosis [168] MTO1 suppresses proliferation and invasion [171] identified to target pri-miR-515, resulting in up-regulation of human epidermal growth factor receptor 2 and enhancement of the therapeutic efficacy of the anti-human epidermal growth factor receptor 2 antibody in breast cancer cells [66]. Likewise, a bisbenzimide analog called targarpremir-210, also called TGP-210, is identified to bind to pre-miR-210, leading to the inhibition of processing of mature miR-210 and suppressing the outgrowth of xenograft tumors in mice [67].…”

Section: Targeting Ncrnas In Cancer Therapymentioning

confidence: 99%

Non-coding RNA in cancer

Yan

2021

Essays in Biochemistry

339

150

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Majority of the human genome is transcribed to RNAs that do not encode proteins. These non-coding RNAs (ncRNAs) play crucial roles in regulating the initiation and progression of various cancers. Given the importance of the ncRNAs, the roles of ncRNAs in cancers have been reviewed elsewhere. Thus, in this review, we mainly focus on the recent studies of the function, regulatory mechanism and therapeutic potential of the ncRNAs including microRNA (miRNA), long ncRNA (lncRNA), circular RNA (circRNA) and PIWI interacting RNA (piRNA), in different type of cancers.

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Circular RNA MTO1 Inhibits the Proliferation and Invasion of Ovarian Cancer Cells Through the miR-182-5p/KLF15 Axis

Cited by 22 publications

References 41 publications

Hsa_circ_0015326 Promotes the Proliferation, Invasion and Migration of Ovarian Cancer Through miR-127-3p/MYB

Hsa_circ_0015326 Promotes the Proliferation, Invasion and Migration of Ovarian Cancer Through miR-127-3p/MYB

<p>Circ-ELF2 Acts as a Competing Endogenous RNA to Facilitate Glioma Cell Proliferation and Aggressiveness by Targeting MiR-510-5p/MUC15 Signaling</p>

Non-coding RNA in cancer

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