Huaier Extract Inhibits Breast Cancer Progression Through a LncRNA-H19/MiR-675-5p Pathway

Wang, Jijun; Wang, Xiaolong; Chen, Tong; Jiang, Liyu; Yang, Qifeng

doi:10.1159/000485093

Cited by 44 publications

(39 citation statements)

References 60 publications

(64 reference statements)

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“…LncRNAs have been found to function as competing endogenous RNAs where they sponge miRNAs and regulate miRNA targets [16]. Wang et al found that Huaier extract inhibited BRCA through lncRNA-H19/miR-675-5p [17]. In the present study, the dysregulated expression of the lncRNA KCNQ1OT1 was found to be significantly associated with BRCA progression.…”

Section: Introductionsupporting

confidence: 57%

The Dysregulated Expression of KCNQ1OT1 and Its Interaction with Downstream Factors miR-145/CCNE2 in Breast Cancer Cells

Feng

Wang

Liang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Next-generation sequencing (NGS) has revealed abundant long noncoding RNAs (lncRNAs) that have been characterized as critical components of cancer biology in humans. The present study aims to investigate the role of the lncRNA KCNQ1OT1 in breast cancer (BRCA) as well as the underlying molecular mechanisms and functions of KCNQ1OT1 involved in the progression of BRCA. Methods: The Cancer Genome Atlas (TCGA) and StarBase v2.0 were used to obtain the required gene data. Dual luciferase reporter gene assays were conducted to verify the relevant intermolecular target relationships. QRT-PCR and Western blot were performed to measure the expression levels of different molecules. Cell proliferation was detected by using the MTT and colony formation assays, while cell migration and invasion were examined by transwell assay. Variations in cell apoptosis and cell cycle were determined through flow cytometry. A tumor xenograft model was applied to assess tumor growth in vivo. Results: KCNQ1OT1 was found to be remarkably highly expressed in BRCA tissues and cells. KCNQ1OT1 modulated CCNE2 through sponging miR-145 in BRCA. KCNQ1OT1 promoted tumor growth in vivo by regulating miR-145/CCNE2. Conclusion: The KCNQ1OT1/miR-145/CCNE2 axis plays a critical regulatory role in BRCA, potentially giving rise to BRCA tumorigenesis and progression. These findings provide valuable evidence for improving the diagnosis and treatment of BRCA in the future.

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Section: Introductionsupporting

confidence: 57%

The Dysregulated Expression of KCNQ1OT1 and Its Interaction with Downstream Factors miR-145/CCNE2 in Breast Cancer Cells

Feng

Wang

Liang

et al. 2018

Cell Physiol Biochem

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“…Considerable studies verified that lncRNAs exert their effects on diverse cancers, such as lung cancer, esophageal squamous cell carcinoma, and breast cancer (Seiler et al, 2017;Wang, Wang, Chen, Jiang, & Yang, 2017;Wu et al, 2017). As a new found lncRNA, MAGI2-AS3 has not been extensively reported in cancers.…”

Section: Discussionmentioning

confidence: 99%

Long noncoding MAGI2‐AS3 promotes colorectal cancer progression through regulating miR‐3163/TMEM106B axis

Ren

Zheng-jun

et al. 2019

Journal Cellular Physiology

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Colorectal cancer (CRC), is mostly derived from normal colon epithelial cells, and has been reported to be one of most common gastrointestinal malignancies globally. An increasing number of researchers have claimed that long noncoding RNAs (lncRNAs) exert significant functions in tumor progression. Nevertheless, the function of MAGI2-AS3 remains uncertain in CRC. The expression of MAGI2-AS3, miR-3163, and transmembrane protein 106B (TMEM106B) messenger RNA was examined by quantitative real-time polymerase chain reaction. Cell apoptosis was measured by caspase-3 activity test. Cell proliferation was tested by cell-counting kit 8 and 5-ethynyl-2′-deoxyuridine assays. Cell migration was detected by transwell assay. Western blot analysis examined the protein expression of TMEM106B. The expression of Ki-67 was evaluated by immunohistochemistry assay. The binding capacity between miR-3163 and MAGI2-AS3 (or TMEM106B) was studied by radioimmunoprecipitation and luciferase reporter assays. The expression of MAGI2-AS3 and TMEM106B was conspicuously upregulated whereas miR-3163 presented lower expression in CRC cells. MAGI2-AS3 deficiency facilitated cell apoptosis but hampered cell proliferation and migration. MAGI2-AS3 combined with miR-3163 and negatively regulated miR-3163 expression. In addition, the administration of sh-MAGI2-AS3 or miR-3163 mimics suppressed CRC cell growth in vivo. Subsequently, miR-3163 targeted TMEM106B and the transfection of sh-MAGI2-AS3 or miR-3163 mimics downregulated TMEM106B expression. Rescue assays verified that TMEM106B overexpression recovered the effects of MAGI2-AS3 inhibition on cell apoptosis, proliferation, and migration in CRC. MAGI2-AS3 drives CRC progression through regulating miR-3163/TMEM106B axis. This supplies innovative insights on the investigation of molecular mechanism in CRC progression. K E Y W O R D S CRC, MAGI2-AS3, miR-3163, TMEM106B

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“…LncRNA-H19/MiR-675-5p Pathway mediated the inhibitory effects of Huaier Extract on BC Progression [42]. MALAT1 induced migration and invasion of human BC cells by competitively binding miR-1 with cdc42 [43].…”

Section: Discussionmentioning

confidence: 98%

LOC101930370/MiR-1471 Axis Modulates the Hedgehog Signaling Pathway in Breast Cancer

Liu

Zhao

Bai

et al. 2018

Cell Physiol Biochem

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Background/Aims: Non-coding RNAs (ncRNAs) play vital regulatory roles in many tumors. However, the functional roles of these transcripts responsible for their dysregulation in breast cancer (BC) are not thoroughly understood. Methods: We examined the expression of microRNA miR-1471 in BC specimens. Online analysis tools predicted that lncRNA LOC101930370 might act as an endogenous ‘sponge’ by competing for miR-1471 binding targets. Luciferase assays were used to prove the interaction of LOC101930370, miR-1471 and SHH. Edu, wound-healing and transwell assays were used to verify the contribution of miR-1471 and LOC101930370 on MCF-7 cells proliferation and metastasis. Gain and loss of function studies were performed to evaluate the relevance of Hedgehog pathway with LOC101930370/miR-1471 regulating axis in MCF-7 cells. Results: The expression of miR-1471 was markedly downregulated in BC. Inhibition of miR-1471 by LOC101930370 was proved by luciferase assay. Knockdown of LOC101930370 suppressed BC cells progression. MiR-1471 inhibitor resulted in a more aggressive metastasis of MCF-7 cells. Moreover, SHH and Gli-1 expression were significantly suppressed by LOC101930370 knockdown, and upregulated by miR-1471 inhibitor transfection. Conclusions: Collectively, our study reveals the interaction between LOC101930370 and miR-1471 for the first time. LOC101930370 positively regulates the expression of SHH by sponging miR-1471, which sheds new light on lncRNA-directed diagnostics and therapeutics in BC.

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Huaier Extract Inhibits Breast Cancer Progression Through a LncRNA-H19/MiR-675-5p Pathway

Cited by 44 publications

References 60 publications

The Dysregulated Expression of KCNQ1OT1 and Its Interaction with Downstream Factors miR-145/CCNE2 in Breast Cancer Cells

The Dysregulated Expression of KCNQ1OT1 and Its Interaction with Downstream Factors miR-145/CCNE2 in Breast Cancer Cells

Long noncoding MAGI2‐AS3 promotes colorectal cancer progression through regulating miR‐3163/TMEM106B axis

LOC101930370/MiR-1471 Axis Modulates the Hedgehog Signaling Pathway in Breast Cancer

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