Post‐transcriptional regulation of <scp>PIAS</scp>3 expression by miR‐18a in malignant mesothelioma

Tian, He; McColl, Karen; Sakre, Nneha; Chen, Yanwen; Wildey, Gary; Dowlati, Afshin

doi:10.1002/1878-0261.12386

Cited by 16 publications

(7 citation statements)

References 42 publications

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“…Zhang et al reported that miR-18a exerts its oncogenic function by regulating the PTEN-PI3K-AKTmTOR signaling axis to improve Cyclin D1 expression and further accelerate cell cycle progression of esophageal squamous cell carcinoma cells [37]. Likewise, miR-18a was found to upregulate PIAS3 expression at the post-transcriptional level to facilitate malignant mesothelioma cell growth [38]. Besides, the deficiency of miR-18a was discovered to improve cisplatin sensitivity to non-small cell lung cancer cells by targeting PTEN [39].…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA GAS5 promotes natural killer cell cytotoxicity against gastric cancer by regulating miR-18a

Wei¹,

Gu²,

Zheng³

et al. 2020

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Natural killer (NK) cells play significant roles in spontaneous antitumor response in multiple cancers, including gastric cancer. Currently, lncRNAs were identified as essential modulators in the development of NK cells via competing for the target miRNA. However, the regulatory mechanism of GAS5 in NK cells remains largely elusive. The expressions of GAS5 and miR-18a in NK cells were measured by qRT-PCR. The killing effects of NK cells were conducted by lactate dehydrogenase (LDH) assay. Detection of IFN-γ and TNF-α level was carried out using ELISA assay. The interaction between GAS5 and miR-18a was determined by the luciferase reporter system and RIP assay, respectively. We found that GAS5 expression was downregulated while miR-18a expression was upregulated in primary NK cells isolated from GC patient compared with the healthy controls. Moreover, activation of NK cells stimulated by IL-2 enhanced the secretion of IFN-γ, TNF-α, and the expression of GAS5. The deficiency of GAS5 significantly suppressed the secretion of IFN-γ and TNF-α as well as the killing effect of NK cells. Subsequently, luciferase reporter and RIP assay confirmed the interaction between GAS5 and miR-18a. In addition, miR-18a inhibitor attenuated GAS5 silencing induced inhibition of the cytotoxicity of activated NK cells. In conclusion, GAS5 promotes the killing effect of the natural killer cells against GC by regulating miR-18a, providing promising strategies for NK cells based antitumor therapies.

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Section: Discussionmentioning

confidence: 99%

Long non-coding RNA GAS5 promotes natural killer cell cytotoxicity against gastric cancer by regulating miR-18a

Wei¹,

Gu²,

Zheng³

et al. 2020

neo

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“…The function of miR‐18a as a suppressor of PIAS3 was also identified in malignant mesothelioma (MM) [66]. The referenced study screened candidate miRNAs in MM cell lines with low PIAS3 expression and conducted luciferase reporter assays to validate the regulation via the 3′‐UTR of PIAS3.…”

Section: Main Textmentioning

confidence: 99%

The dual functional role of MicroRNA‐18a (miR‐18a) in cancer development

Shen

Cao

Zhu

et al. 2019

Clinical & Translational Med

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The polycistronic miR‐17‐92 cluster is instrumental in physiological processes commonly dysregulated in cancer, such as proliferation, the cell cycle, apoptosis, and differentiation. MicroRNA‐18a (miR‐18a) is one of the most conserved and multifunctional miRNAs in the cluster and is frequently overexpressed in malignant tumors. Altered miR‐18a expression has been found in various physiological and pathological processes, including cell proliferation, apoptosis, epithelial–mesenchymal transition (EMT), tumorigenesis, cancer invasion and metastasis. In this review, we summarized the molecular basis and regulatory targets of miR‐18a in cancer development. Interestingly, miR‐18a has a dual functional role in either promoting or inhibiting oncogenesis in different human cancers. The differential miRNA expression in cancers of the same organ at different stages or of various subtypes suggests that this dual function of miR‐18a is independent of cancer type and may be attributed to the fundamental differences in tumorigenic mechanisms. Finally, we summarized the current clinical use of miR‐18a and discussed its potential uses in cancer therapy.

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“…In our previous comprehensive analysis of miRNA expression by RT-qPCR using TaqMan Low Density Array Human miRNA Cards, both miR-18a-3p and miR-18a-5p were upregulated in malignant mesothelioma cell lines (ACC-MESO1, ACC-MESO4, CRL-2081, CRL-5820, CRL-5826, CRL-5915, and CRL-5946) compared to non-neoplastic mesothelial tissues (11). He et al (26) found that miR-18a-5p promoted mesothelioma cell proliferation by downregulating PIAS3, but little is known about the function of miR-18a-3p in mesothelioma cells. In the present study, we showed that inhibition of miR-18a-3p reduced proliferation and migration, but increased apoptosis of mesothelioma cells.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of miR‑18a‑3p reduces proliferation of mesothelioma cells and sensitizes them to cisplatin

et al. 2020

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Malignant pleural mesothelioma is a notorious human malignancy. Despite combination chemotherapy with cisplatin and pemetrexed, the majority of patients with advanced malignant pleural mesothelioma have a poor prognosis. MicroRNAs (miRNAs/miRs) are short non-coding RNAs that regulate various biological processes by binding to the 3'-untranslated region of target gene mRNAs and suppressing their expression. Since abnormal expression patterns of miRNAs are a common feature in human malignancies, a number of them have been researched as potential therapeutic targets. Our previous study demonstrated that microRNA-18a (miR-18a) is upregulated in mesothelioma cell lines compared with in non-neoplastic mesothelial tissues, but its function remains unclear. In the present study, miRNA inhibitor was transfected into mesothelioma cell lines and then analyzed various cellular functions. Mesothelioma cells transfected with the miR-18a inhibitor exhibited lower proliferation and migration rates compared with cells transfected with a negative control inhibitor in proliferation and wound scratch assays, respectively. Additionally, the present study revealed that downregulation of miR-18a increased mesothelioma cell apoptosis. In a chemosensitivity assay, transfection of the miR-18a inhibitor significantly increased the sensitivity of mesothelioma cells to cisplatin but not to pemetrexed. Therefore, miR-18a may be a potential therapeutic target for mesothelioma resistant to cisplatin. Materials and methods Mesothelioma cell lines. Four human mesothelioma cell lines were used in this study. Two cell lines (ACC-MESO1 and ACC-MESO4) were purchased from the RIKEN BioResearch Center (Tsukuba, Japan) (15) and the other two (CRL-5915 and CRL-5946) were purchased from the American Type Culture Collection. Cells were cultured with Roswell Park Memorial

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Post‐transcriptional regulation of PIAS3 expression by miR‐18a in malignant mesothelioma

Cited by 16 publications

References 42 publications

Long non-coding RNA GAS5 promotes natural killer cell cytotoxicity against gastric cancer by regulating miR-18a

Long non-coding RNA GAS5 promotes natural killer cell cytotoxicity against gastric cancer by regulating miR-18a

The dual functional role of MicroRNA‐18a (miR‐18a) in cancer development

Inhibition of miR‑18a‑3p reduces proliferation of mesothelioma cells and sensitizes them to cisplatin

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