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      By downregulating TIAM1 expression, microRNA-329 suppresses gastric cancer invasion and growth

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          Abstract

          Gastric cancer (GC) is one of the most common malignant tumors worldwide. Emerging evidence has shown that abnormal microRNAs (miRNAs) expression is involved in tumorigenesis. MiR-329 was previously reported to act as a tumor suppressor or oncogene in some types of cancer. However, its function in gastric cancer (GC) is unclear. Here, we found that miR-329 was down-regulated in GC compared with adjacent controls. Enforced expression of miR-329 inhibited proliferation, migration and invasion of gastric cancer cells in vitro. We identified T lymphoma invasion and metastasis 1 (TIAM1) gene as potential target of miR-329. MiR-329 levels inversely correlated with TIAM1 expression in GC. Importantly, TIAM1 rescued the miR-329-mediated inhibition of cell invasion and proliferation. Finally, reintroduction of miR-329 significantly inhibited tumor formation of GC in the xenograft mice. Our findings suggest that miR-329 is a tumor suppressor and potential therapeutic target of GC

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          Incidence and mortality of gastric cancer in China.

          Ling Yang (2006)
          Gastric cancer is one of the most frequent cancers in the world; almost two-thirds of gastric cancer cases and deaths occur in less developed regions. In China, based on two national mortality surveys conducted in 1970s and 1990s, there is an obvious clustering of geographical distribution of gastric cancer in the country, with the high mortality being mostly located in rural areas, especially in Gansu, Henan, Hebei, Shanxi and Shaanxi Provinces in the middle-western part of China. Despite a slight increase from the 1970s to early 1990s, remarkable declines in gastric cancer mortality were noticed in almost the entire population during the last decade in China. These declines were largely due to the dramatic improvements in the social-economic environment, lifestyle, nutrition, education and health care system after economic reforms started two decades ago. Nevertheless, gastric cancer will remain a significant cancer burden currently and be one of the key issues in cancer prevention and control strategy in China. It was predicted that, in 2005, 0.3 million deaths and 0.4 million new cases from gastric cancer would rank the third most common cancer. The essential package of the prevention and control strategy for gastric cancer in China would focus on controlling Helicobacter pylori (H. pylori) infection, improving educational levels, advocating healthy diet and anti-tobacco campaign, searching for cost-effective early detection, diagnosis and treatment programs including approaches for curable management and palliative care.
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            miRNA-223 promotes gastric cancer invasion and metastasis by targeting tumor suppressor EPB41L3.

            Xiaohua Li, Ying. Zhang, Hongwei Zhang … (2011)
            Traditional research modes aim to find cancer-specific single therapeutic target. Recently, emerging evidence suggested that some micro-RNAs (miRNA) can function as oncogenes or tumor suppressors. miRNAs are single-stranded, small noncoding RNA genes that can regulate hundreds of downstream target genes. In this study, we evaluated the miRNA expression patterns in gastric carcinoma and the specific role of miR-223 in gastric cancer metastasis. miRNA expression signature was first analyzed by real-time PCR on 10 paired gastric carcinomas and confirmed in another 20 paired gastric carcinoma tissues. With the 2-fold expression difference as a cutoff level, we identified 22 differential expressed mature miRNAs. Sixteen miRNAs were upregulated in gastric carcinoma, including miR-223, miR-21, miR-23b, miR-222, miR-25, miR-23a, miR-221, miR-107, miR-103, miR-99a, miR-100, miR-125b, miR-92, miR-146a, miR-214 and miR-191, and six miRNAs were downregulated in gastric carcinoma, including let-7a, miR-126, miR-210, miR-181b, miR-197, and miR-30aa-5p. After examining these miRNAs in several human gastric originated cell lines, we found that miR-223 is overexpressed only in metastatic gastric cancer cells and stimulated nonmetastatic gastric cancer cells migration and invasion. Mechanistically, miR-223, induced by the transcription factor Twist, posttranscriptionally downregulates EPB41L3 expression by directly targeting its 3'-untranslated regions. Significantly, overexpression of miR-223 in primary gastric carcinomas is associated with poor metastasis-free survival. These findings indicate a new regulatory mode, namely, specific miRNA, which is activated by its upstream transcription factor, could suppress its direct targets and lead to tumor invasion and metastasis. ©2011 AACR.
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              MicroRNA-25 regulates chemoresistance-associated autophagy in breast cancer cells, a process modulated by the natural autophagy inducer isoliquiritigenin

              Zhiyu Wang, Neng Wang, Pengxi Liu … (2014)
              Recent findings have revealed that dysregulated miRNAs contribute significantly to autophagy and chemoresistance. Pharmacologically targeting autophagy-related miRNAs is a novel strategy to reverse drug resistance. Here, we report a novel function of isoliquiritigenin (ISL) as a natural inhibitor of autophagy-related miR-25 in killing drug-resistant breast cancer cells. ISL induced chemosensitization, cell cycle arrest and autophagy, but not apoptosis, in MCF-7/ADR cells. ISL also promoted the degradation of the ATP-binding cassette (ABC) protein ABCG2 primarily via the autophagy-lysosome pathway. More importantly, miRNA 3.0 array experiments identified miR-25 as the main target of ISL in triggering autophagy flux. A mechanistic study validated that miR-25 inhibition led to autophagic cell death by directly increasing ULK1 expression, an early regulator in the autophagy induction phase. miR-25 overexpression was demonstrated to block ISL-induced autophagy and chemosensitization. Subsequent in vivo experiments showed that ISL had chemosensitizing potency, as revealed by an increase in LC3-II staining, the downregulation of ABCG2, a reduction in miR-25 expression and the activation of the miR-25 target ULK1. Overall, our results not only indicate that ISL acts as a natural autophagy inducer to increase breast cancer chemosensitivity, but also reveal that miR-25 functions as a novel regulator of autophagy by targeting ULK1.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Oncotarget
                Journal ID (iso-abbrev): Oncotarget
                Journal ID (publisher-id): ImpactJ
                Title: Oncotarget
                Publisher: Impact Journals LLC
                ISSN (Electronic): 1949-2553
                Publication date Collection: 10 July 2015
                Publication date (Electronic): 19 February 2015
                Volume: 6
                Issue: 19
                Pages: 17559-17569
                Affiliations
                1 Department of Orthopaedic Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China
                2 Department of Abdominal Surgery, Cancer Institute and Cancer Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China
                3 Department of Anaesthesia and Intensive Care, The Chinese University of Hong Kong, Hong Kong, China
                Author notes
                Correspondence to: Jianxiong Shen, shenjianxiong@ 123456medmail.com.cn
                Article
                DOI: 10.18632/oncotarget.2755
                PMC ID: 4627328
                PubMed ID: 25654811
                SO-VID: 43273d03-4d28-42cc-af30-645bff98cd5a
                Copyright © Copyright: © 2015 Li et al.
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                Date received : 9 November 2014
                Date accepted : 16 November 2014
                Categories
                Subject: Research Paper

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: gastric cancer,micrornas,mir-329,tiam1
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: gastric cancer, micrornas, mir-329, tiam1

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