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      M2 Macrophages Promote HCC Cells Invasion and Migration via miR-149-5p/MMP9 Signaling

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          The roles of M2 macrophages on promoting tumor progression and chemotherapy resistance have been well studied in many cancers, such as pancreatic cancer, kidney cancer and so on, but its linkage to HCC cells still remains unclear. Here we found that M2 macrophages could alter miR-149-5p to increase MMP9 expression in HCC cells and mechanism dissection revealed that miR-149-5p might directly target the 3'UTR of MMP9-mRNA to suppress its translation. The in vivo orthotopic xenografts mouse model with oemiR-149-5p also validated in vitro data. Together, these findings suggest that M2 macrophages may through altering the miR-149-5p to promote HCC progression and targeting the M2 macrophages/miR149-5P/MMP9 signaling may help in the development of the novel therapies to better suppress the HCC progression.

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          Most cited references 19

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          Distinct role of macrophages in different tumor microenvironments.

          Macrophages are prominent in the stromal compartment of virtually all types of malignancy. These highly versatile cells respond to the presence of stimuli in different parts of tumors with the release of a distinct repertoire of growth factors, cytokines, chemokines, and enzymes that regulate tumor growth, angiogenesis, invasion, and/or metastasis. The distinct microenvironments where tumor-associated macrophages (TAM) act include areas of invasion where TAMs promote cancer cell motility, stromal and perivascular areas where TAMs promote metastasis, and avascular and perinecrotic areas where hypoxic TAMs stimulate angiogenesis. This review will discuss the evidence for differential regulation of TAMs in these microenvironments and provide an overview of current attempts to target or use TAMs for therapeutic purposes.
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            Hypoxia, lipids, and cancer: surviving the harsh tumor microenvironment.

            Solid tumors typically develop hostile microenvironments characterized by irregular vascularization and poor oxygen (O2) and nutrient supply. Whereas normal cells modulate anabolic and catabolic pathways in response to changes in nutrient availability, cancer cells exhibit unregulated growth even under nutrient scarcity. Recent studies have demonstrated that constitutive activation of growth-promoting pathways results in dependence on unsaturated fatty acids for survival under O2 deprivation. In cancer cells, this dependence represents a critical metabolic vulnerability that could be exploited therapeutically. Here we review how this dependence on unsaturated lipids is affected by the microenvironmental conditions faced by cancer cells. Copyright © 2014 Elsevier Ltd. All rights reserved.
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              Alternatively activated (M2) macrophages promote tumour growth and invasiveness in hepatocellular carcinoma.

              The roles of alternatively activated (M2) macrophages on pro-tumour phenotypes have been well documented in many cancers except hepatocellular carcinoma (HCC). Considering their close relationship with chronic tissue injuries as well as enhanced tumour invasiveness and growth, we aimed to investigate the direct effects of M2 macrophages on HCC.

                Author and article information

                J Cancer
                J Cancer
                Journal of Cancer
                Ivyspring International Publisher (Sydney )
                1 January 2020
                : 11
                : 5
                : 1277-1287
                [1 ]Department of Biliary and Pancreatic Surgery, Xiangya Hospital, Central South University, Changsha, 410008, China.
                [2 ]Department of Urology, Shanghai Tenth People's Hospital, School of Medicine in Tongji University, Shanghai, China.
                [3 ]Department of Liver Surgery, Xiangya Hospital, Central South University, Changsha, 410008, China.
                [4 ]CITIC Xiangya Reproductive and Genetic Specialist Hospital, Changsha, 410008, China.
                [5 ]Department of Hepatobiliary and Pancreatic Surgery, Xiangya Hospital, Central South University, Changsha, 410008, China.
                Author notes
                ✉ Corresponding authors: Yao Xiao (Email: yaoxiao@ 123456csu.edu.cn ) and Yixiong Li (Email: liyixiong2011@ 123456163.com ).

                Competing Interests: The authors have declared that no competing interest exists.

                © The author(s)

                This is an open access article distributed under the terms of the Creative Commons Attribution License ( https://creativecommons.org/licenses/by/4.0/). See http://ivyspring.com/terms for full terms and conditions.

                Research Paper

                Oncology & Radiotherapy

                liver cancer, mirna-149-5p, mmp9, invasion, migration


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