MicroRNA-139-3p Inhibits the Growth and Metastasis of Ovarian Cancer by Inhibiting ELAVL1 [Retraction]

Xue, Fu‐Shan; Li, Qi Rong; Xu, Yan; Zhou, Hai

doi:10.2147/ott.s384255

Cited by 3 publications

(5 citation statements)

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“…And as reported miRNA-139-3p generally works as tumor suppressor. For example, Xue et al [22] demonstrated that overexpressed miRNA-139-3p could effectively repress the progression of ovarian cancer. In accordance with previous reports, we first obtained the significantly low expression of miRNA-139-3p in BUC tissues through the bioinformatics database, which was validated by qRT-PCR experiment in BUC tissues and cell lines.…”

Section: Discussionmentioning

confidence: 99%

“…Growing evidence has proved that miRNAs function as a pivotal part in tumor development by modulating their target genes at expression level. The abnormal expression of miRNA-139-3p in different cancers, such as ovarian cancer [22], HCC [12], glioma [23] and breast cancer [21], is intensively investigated. And as reported miRNA-139-3p generally works as tumor suppressor.…”

Section: Discussionmentioning

confidence: 99%

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MiRNA-139-3p inhibits malignant progression in urothelial carcinoma of the bladder via targeting KIF18B and inactivating Wnt/beta-catenin pathway

Zhang

Liu

2022

Pharmacogenetics and Genomics

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Objective Bladder cancer is a highly prevalent disease worldwide. We aimed to investigate the effect of miRNA/mRNA signaling on bladder urothelial carcinoma (BUC). Methods MiRNA-139-3p wasselected from The Cancer Genome Atlas database, and its downstream target gene was predicted. The correlation between miRNA-139-3p and intersected mRNAs was analyzed. The mRNA expression levels of miRNA-139-3p and KIF18B in BUC were assayed via quantitative real-time polymerase chain reaction. Effects of miRNA-139-3p on cell proliferation, invasion, migration and cell cycle were detected via Cell Counting Kit-8, colony formation, transwell, wound healing and flow cytometry assays, respectively. Binding relationship between miRNA-139-3p and KIF18B was verified by dual-luciferase reporter gene detection. The protein expression levels of KIF18B, β-catenin and Cyclin D1 were detected by Western blot. Rescue assays were performed for verifying the interaction among miRNA-139-3p, KIF18B and Wnt/β-catenin signaling pathway, which revealed effects of miRNA-139-3p/KIF18B on BUC cells. Results MiRNA-139-3p was remarkably underexpressed, and KIF18B was dramatically overexpressed in BUC cells, respectively. It was also demonstrated that overexpressing miRNA-139-3p could prominently inhibit proliferation, invasion and migration of BUC, and block BUC cells at G0-G1 phase. Afterwards, we found that miRNA-139-3p could bind to KIF18B mRNA 3′UTR, and miRNA-139-3p had a negative regulatory effect with KIF18B. Subsequent experimental results presented that overexpressing KIF18B could reverse inhibitory effect of overexpressing miRNA-139-3p on BUC. Finally, this study also ascertained that miRNA-139-3p/KIF18B could repress oncogenic effects of BUC via modulating Wnt/β-catenin signaling pathway. Conclusion MiRNA-139-3p/KIF18B/Wnt/β-catenin could significantly inhibit the malignant progression of BUC, and its targeting mechanism might provide an effective therapeutic target for BUC patients.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

MiRNA-139-3p inhibits malignant progression in urothelial carcinoma of the bladder via targeting KIF18B and inactivating Wnt/beta-catenin pathway

Zhang

Liu

2022

Pharmacogenetics and Genomics

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“…6 Additionally, the upregulated expression of ELAVL1 has been found in several human malignant tumours. 8,11 ELAVL1 usually acts as a tumour promoter due to its proliferative and antiapoptotic effects. 28 In fact, ELAVL1 is a key mediator during the growth and metastasis of cancer.…”

Section: Discussionmentioning

confidence: 99%

“…10 Moreover, previous studies have indicated that ELAVL1 can participate in the occurrence of malignant tumours. 11 However, knowledge on the role of ELAVL1 in the resistance of CC cells to ionizing radiation (IR) is very limited.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‐324‐5p affects the radiotherapy response of cervical cancer via targeting ELAV‐like RNA binding protein 1

Fan

Yang

et al. 2020

The Kaohsiung J of Med Scie

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Cervical cancer (CC) seriously threatens the health of women. Radiation therapy (RT) is the major treatment for CC. However, the recurrent CC can acquire resistance to RT. Thus, it is necessary to find a new method for reversing RT resistance in CC. It has been reported that miR‐324‐5p can suppress the progression of multiple cancers. However, whether it can reverse resistance to RT in CC remains unclear. qRT‐PCR and Western blotting were used to detect gene and protein expression in CC cells, respectively. Cell proliferation was tested by CCK‐8 assay and colony formation assay. In addition, cell apoptosis was detected by flow cytometry. Transwell assays were performed to detect cell migration. Dual luciferase reporter assay and TargetScan were used to explore the targets of microRNA‐324‐5p (miR‐324‐5p). MiR‐324‐5p was downregulated in CC cells. Overexpression of miR‐324‐5p sensitized CC cells to RT. In addition, miR‐324‐5p mimics significantly induced apoptosis and inhibits the migration of CC cells in the presence of 137Cs ionizing radiation. Furthermore, miR‐324‐5p sensitized CC cells to ionizing radiation by targeting ELAV‐like RNA binding protein 1 (ELAVL1). MiR‐324‐5p overexpression affects the radiotherapy response of CC by targeting ELAVL1, which may serve as a new target for the treatment of CC.

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“…ELAVL1 participates in a variety of tumor biological processes as an oncogene. Studies showed that ELAVL1 promoted the progression of liver cancer [160], lung cancer [161][162][163], colorectal cancer [164][165][166], gastric cancer [36], esophageal cancer [167], breast cancer [168,169], prostate cancer [170,171], and ovarian cancer [172]. However, few studies have investigated whether the effect of ELAVL1 on the expression of downstream molecules relies on m6A, and the role played by ELAVL1 in tumors is unclear.…”

Section: Readersmentioning

confidence: 99%

Role of m6A writers, erasers and readers in cancer

et al. 2022

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The N(6)-methyladenosine (m6A) modification is the most pervasive modification of human RNAs. In recent years, an increasing number of studies have suggested that m6A likely plays important roles in cancers. Many studies have demonstrated that m6A is involved in the biological functions of cancer cells, such as proliferation, invasion, metastasis, and drug resistance. In addition, m6A is closely related to the prognosis of cancer patients. In this review, we highlight recent advances in understanding the function of m6A in various cancers. We emphasize the importance of m6A to cancer progression and look forward to describe future research directions.

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MicroRNA-139-3p Inhibits the Growth and Metastasis of Ovarian Cancer by Inhibiting ELAVL1 [Retraction]

Cited by 3 publications

References 0 publications

MiRNA-139-3p inhibits malignant progression in urothelial carcinoma of the bladder via targeting KIF18B and inactivating Wnt/beta-catenin pathway

MiRNA-139-3p inhibits malignant progression in urothelial carcinoma of the bladder via targeting KIF18B and inactivating Wnt/beta-catenin pathway

MicroRNA‐324‐5p affects the radiotherapy response of cervical cancer via targeting ELAV‐like RNA binding protein 1

Role of m6A writers, erasers and readers in cancer

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