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Tumor?suppressive miR?299?3p inhibits gastric cancer cell invasion by targeting heparanase.

ABSTRACT: Gastric cancer (GC) remains a leading cause of cancer?associated mortality globally. Emerging evidence suggests that microRNAs (miRs) function as oncogenes or tumor suppressors, contributing to various aspects of cancer progression, including invasion and metastasis. In the present study, the specific role of miR?299?3p in the invasion of GC cells was investigated. The expression level of miR?299?3p was measured using reverse transcription?quantitative PCR and in situ hybridization in human GC tissues. Effects of miR?299?3p on GC cell invasion were determined by Transwell assay. Bioinformatics and luciferase reporter assays were performed to identify and verify the downstream effectors of miR?299?3p. miR?299?3p expression analysis in clinical GC samples revealed a significant downregulation of miR?299?3p compared with non?tumor tissues. Inhibition of miR?299?3p promoted the invasive abilities of GC cells, whereas its overexpression significantly suppressed cell invasion. Bioinformatics and luciferase reporter assays identified heparanase (HPSE) as a direct target of miR?299?3p, the ectopic expression of which reversed the impairment in cell invasion induced by miR?299?3p upregulation. Furthermore, HPSE expression was negatively associated with miR?299?3p levels in human GC tissues. Overall, the present study indicated that miR?299?3p functions as a tumor suppressor by directly targeting HPSE, highlighting its potential as a target for the treatment of GC.

SUBMITTER: Zhou X

PROVIDER: S-EPMC6691259 | biostudies-literature | 2019 Sep

REPOSITORIES: biostudies-literature

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Tumor‑suppressive miR‑299‑3p inhibits gastric cancer cell invasion by targeting heparanase.

Zhou Xiangjun X Hu Mengmou M Ge Zhenghui Z

Molecular medicine reports 20190627 3

Gastric cancer (GC) remains a leading cause of cancer‑associated mortality globally. Emerging evidence suggests that microRNAs (miRs) function as oncogenes or tumor suppressors, contributing to various aspects of cancer progression, including invasion and metastasis. In the present study, the specific role of miR‑299‑3p in the invasion of GC cells was investigated. The expression level of miR‑299‑3p was measured using reverse transcription‑quantitative PCR and in situ hybridization in human GC t ...[more]

PMID: 31257534

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Project description:Objective:Mounting research has established the role of microRNAs (miRNAs) as oncogenes or anti-oncogenes (tumor suppressors) in the development and progression of several cancers. The purpose of our current study is to delineate the roles and functional mechanisms of miR-331-3p and MLLT10 in non-small cell lung cancer (NSCLC) tumorigenesis. Patients and Methods:Quantitative reverse transcription-polymerase chain reaction (RT-qPCR) was employed to measure miR-331-3p expression levels in twenty-six matched tumor tissues and non-cancerous tissues collected from patients suffering from NSCLC, and from six NSCLC cell lines separately: A549, H1650, H292, H1299, H1944 and BEAS-2b. We employed the dual-luciferase activity assay to check whether the putative gene, MLLT10, was a downstream target of miR-331-3p in NSCLC pathogenesis and development. Western blot was conducted to analyze the protein expression levels of MLLT10 (AF10), E-cadherin, Vimentin, and GAPDH. CCK-8 assay, transwell migration assay, and transwell invasion assay were carried out to observe the functions of miR-331-3p and MLLT10 on NSCLC tumor cell proliferation, metastasis, and invasion, respectively. To identify whether the metastasis of NSCLC tumor cells was EMT-mediated, supplementary experiments involving E-cadherin and Vimentin were implemented. Results:miR-331-3p was downregulated in NSCLC, which promoted tumor cell proliferation, whereas the overexpression of miR-331-3p inhibited tumor cell proliferation. Being a direct target of miR-331-3p, MLLT10 was negatively modulated by miR-331-3p, which suppressed tumor cell proliferation, migration, and invasion in NSCLC. However, MLLT10 overexpression alleviated the above inhibitory effects. Furthermore, EMT-mediated metastasis was proved to be present in NSCLC. Conclusion:miR-331-3p played a suppressor role in NSCLC tumor cell proliferation, EMT-mediated metastasis, and invasion by targeting MLLT10. Our findings highlighted that miR-331-3p/MLLT10 axis could be useful as a clinical diagnostic marker and therapeutic target in NSCLC patients.

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Tumor?suppressive miR?299?3p inhibits gastric cancer cell invasion by targeting heparanase.

Publications

Tumor‑suppressive miR‑299‑3p inhibits gastric cancer cell invasion by targeting heparanase.

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