miR-188-5p Suppresses Gastric Cancer Cell Proliferation and Invasion via Targeting ZFP91

Peng, Yu‐Ping; Shen, Xiaoxia; Jiang, Honggang; Chen, Zhiheng; Wu, Jiaming; Zhu, Yi; Zhou, Yuan; Jin, Li

doi:10.3727/096504018x15191223015016

Cited by 51 publications

(47 citation statements)

References 29 publications

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“…The results of luciferase reporter and RNA pull-down assays showed that miR-188-5p was a direct target of SBF2-AS. MiR-188-5p has been identified to be significantly decreased in multiple cancers, including hepatocellular carcinoma [24], gastric cancer [25], and prostate cancer [26]. Likewise, our data also confirmed that miR-188-5p was a tumor suppressor in AML.…”

Section: Discussionsupporting

confidence: 82%

Long noncoding RNA SBF2-AS1 act as a ceRNA to modulate cell proliferation via binding with miR-188-5p in acute myeloid leukemia

Tian

Wang

Xiao

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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LncRNA SBF2-AS1 has been reported to be implicated in the deterioration of multiple human cancers. However, the roles and underlying mechanisms of SBF2-AS1 in acute myeloid leukemia (AML) are still unclear. In the present study, the online GEPIA database showed that SBF2-AS1 expression was significantly increased in AML samples. QRT-PCR results showed that SBF2-AS1 expression was upregulated in AML cells. CCK-8 assay revealed that SBF2-AS1 inhibition decreased AML cells proliferation ability in vitro. Flow cytometry assays showed that SBF2-AS1 inhibition induced AML cells apoptosis and arrested AML cells in G0/G1 phase. Mechanistically, miR-188-5p was identified as a direct target of SBF2-AS1. SBF2-AS1 upregulated the expression level of ZFP91 by sponging miR-188-5p. And the effects of SBF2-AS1 suppression on AML cells progression could be abolished by miR-188-5p inhibitors. Moreover, we found that SBF2-AS1 inhibition reduced tumor growth in vivo. Taken together, our findings elucidated that SBF2-AS1 could act as a miRNA sponge in AML progression, and provided a potential therapeutic strategy for AML treatment.

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Section: Discussionsupporting

confidence: 82%

Long noncoding RNA SBF2-AS1 act as a ceRNA to modulate cell proliferation via binding with miR-188-5p in acute myeloid leukemia

Tian

Wang

Xiao

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…To date, most of the research has revealed that miR-188-5p acts as a tumor suppressor in human cancers. In line with these previous reports (Fang et al, 2015;Peng et al, 2018;Zhang et al, 2018), miR-188-5p also plays a tumorsuppressive function in breast cancer progression, thus having potential therapeutic value in breast cancer. miRNAs are key gene expression regulators.…”

Section: Discussionsupporting

confidence: 85%

miR‐188‐5p suppresses cellular proliferation and migration via IL6ST: A potential noninvasive diagnostic biomarker for breast cancer

Wang

Zhang

Yang

et al. 2019

Journal Cellular Physiology

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Previously, serum miR-188-5p is differentially expressed in breast cancer, but the diagnostic potential of circulating miR-188-5p as well as its regulatory mechanism in breast cancer remain uncertain. Herein, serum miR-188-5p was detected by real-time polymerase chain reaction in patients with breast cancer, breast fibroadenoma, and healthy subjects.Circulating miR-188-5p was abnormally elevated in patients with breast cancer as compared with these other two groups, and was reduced in patients with breast cancer following surgical treatment. Increased serum miR-188-5p corresponded to lymph node metastasis status and TNM stages of breast cancer. A receiver operating characteristic curve analysis of the ability to circulate miR-188-5p to distinguish between patients with breast cancer and either noncancerous patients or patients with breast fibroadenoma yielded corresponding areas under the curve of 0.894 and 8.814. miR-188-5p was downregulated in the highly malignant cancer line MDA-MB-231 relative to the less malignant MCF-7 cells. In vitro, functional analyses conducted via transfecting cells with mimics and inhibitors revealed miR-188-5p to suppress breast cancer cell proliferation and migration, which was mediated by its downstream target IL6ST. Comparison of intracellular and exosomal miR-188-5p levels indicated that miR-188-5p was selectively sorted into exosomes derived from MDA-MB-231 cells rather than those from MCF-7 cells. However, exosomal miR-188-5p levels in the serum of patients with breast cancer were reduced compared to healthy controls and did not differ relative to patients with breast fibroadenoma. In summary, miR-188-5p acts in a tumor-suppressive manner in breast cancer progression and may serve as a noninvasive early diagnostic biomarker and therapeutic target in breast cancer.

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“…39,40 Peng et al showed that ZEP91 was a target of miR-188-5p and together with it regulated GC cell proliferation and invasion. 41 In our study, ZFP91 was a target mRNA of miR-22-3p and overexpression of ZFP91 could alleviate the inhibitory effect of overexpression of miR-22-3p on GC/OXA cells. Besides, we also found that MALAT1 regulated ZFP91 expression by completely binding miR-22-3p in GC/OXA cells.…”

Section: Discussionmentioning

confidence: 52%

<p>lncRNA MALAT1 modulates oxaliplatin resistance of gastric cancer via sponging miR-22-3p</p>

Zhang

2020

OTT

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Objective: Various regulatory mechanisms have been demonstrated to be associated with cancer progression. ncRNA and mRNA play important roles in gastric cancer (GC) cell growth and drug resistance, respectively. However, the regulatory network of ncRNA and mRNA in GC oxaliplatin (OXA) resistance has not been fully clarified. Methods: The expression of miR-22-3p, MALAT1, and zinc finger protein 91 (ZFP91) was detected in tissues and cells using quantitative real-time PCR. The protein level of ZFP91 was measured by Western blot analysis. Luciferase reporter, pull-down, and RNA immunoprecipitation assays were used to determine the relationship between MALAT1, miR-22-3p, and ZFP91. MTT assay was applied to measure cell survival and proliferation. Cell apoptosis was detected using flow cytometry. Tumor xenograft assay was used to detect the function of miR-22-3p in vivo. Results: In this study, we found that MALAT1 and ZFP91 expression was upregulated while the expression of miR-22-3p was downregulated in GC/OXA tissues and cells. Additionally, miR-22-3p was a target miRNA of MALAT1 and ZFP91 was a target mRNA of miR-22-3p. Functional studies showed that the knockdown of MALAT1 or overexpression of miR-22-3p inhibited GC/OXA cell survival, proliferation, and drug resistance as well as induced apoptosis, which could be reversed by the inhibition of miR-22-3p or overexpression of ZFP91. Conclusion: We observed a new regulatory network for MALAT1 in drug resistance of GC. MALAT1 modulates ZFP91 to promote GC cells OXA resistance via sponging miR-22-3p.

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miR-188-5p Suppresses Gastric Cancer Cell Proliferation and Invasion via Targeting ZFP91

Cited by 51 publications

References 29 publications

Long noncoding RNA SBF2-AS1 act as a ceRNA to modulate cell proliferation via binding with miR-188-5p in acute myeloid leukemia

Long noncoding RNA SBF2-AS1 act as a ceRNA to modulate cell proliferation via binding with miR-188-5p in acute myeloid leukemia

miR‐188‐5p suppresses cellular proliferation and migration via IL6ST: A potential noninvasive diagnostic biomarker for breast cancer

<p>lncRNA MALAT1 modulates oxaliplatin resistance of gastric cancer via sponging miR-22-3p</p>

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