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      OncoTargets and Therapy (submit here)

      This international, peer-reviewed Open Access journal by Dove Medical Press focuses on the pathological basis of cancers, potential targets for therapy and treatment protocols to improve the management of cancer patients. Publishing high-quality, original research on molecular aspects of cancer, including the molecular diagnosis, since 2008. Sign up for email alerts here. 50,877 Monthly downloads/views I 4.345 Impact Factor I 7.0 CiteScore I 0.81 Source Normalized Impact per Paper (SNIP) I 0.811 Scimago Journal & Country Rank (SJR)

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      Stanniocalcin 1 in tumor microenvironment promotes metastasis of ovarian cancer

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          Abstract

          Background: Tumor metastasis is the major challenge for ovarian cancer treatment. Cancer-associated fibroblasts (CAFs), a major component existing in tumor microenvironment, can secrete several cytokines to interact with cancer epithelial cells, and promote cancer metastasis. Stanniocalcin 1 (STC1), a secretory glycoprotein hormone, has been proven to be an important factor in ovarian tumorigenesis.

          Methods: In this study, we focused on the functional role of STC1 in ovarian cancer microenvironment, investigated STC1’s effects on the proliferation and metastasis of ovarian cancer cells, and explored the molecular mechanism underlying STC1-mediated cancer metastasis.

          Results: By analyzing the GEO dataset and examined STC1 expression in CAFs isolated from ovarian cancer patients, we found that expression of STC1 was higher in ovarian cancer stroma and CAFs than in the normal ovarian stroma and normal fibroblasts (NFs). Addition of recombinant human STC1 (rhSTC1) promoted cell proliferation and metastasis in ovarian cancer, while adoption of STC1 neutralizing antibody (STC1 Ab) abolished the effects. Furthermore, our results revealed that STC1 promoted the phosphorylation of Akt (Ser473), and upregulated several epithelial–mesenchymal transition (EMT) markers including fibronectin，vimentin and slug. In addition, we demonstrated that STC1 in tumor microenvironment could mediate the conversion of NFs to CAFs.

          Conclusion: Taken together, the study results suggested the crucial role of STC1 in tumor environment on the metastasis of ovarian cancer.

          Most cited references14

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          MicroRNAs reprogram normal fibroblasts into cancer-associated fibroblasts in ovarian cancer.

          Anirban Mitra, Marion R Zillhardt, Youjia Hua … (2012)
          Cancer-associated fibroblasts (CAF) are a major constituent of the tumor stroma, but little is known about how cancer cells transform normal fibroblasts into CAFs. microRNAs (miRNA) are small noncoding RNA molecules that negatively regulate gene expression at a posttranscriptional level. Although it is clearly established that miRNAs are deregulated in human cancers, it is not known whether miRNA expression in resident fibroblasts is affected by their interaction with cancer cells. We found that in ovarian CAFs, miR-31 and miR-214 were downregulated, whereas miR-155 was upregulated when compared with normal or tumor-adjacent fibroblasts. Mimicking this deregulation by transfecting miRNAs and miRNA inhibitors induced a functional conversion of normal fibroblasts into CAFs, and the reverse experiment resulted in the reversion of CAFs into normal fibroblasts. The miRNA-reprogrammed normal fibroblasts and patient-derived CAFs shared a large number of upregulated genes highly enriched in chemokines, which are known to be important for CAF function. The most highly upregulated chemokine, CCL5, (C-C motif ligand 5) was found to be a direct target of miR-214. These results indicate that ovarian cancer cells reprogram fibroblasts to become CAFs through the action of miRNAs. Targeting these miRNAs in stromal cells could have therapeutic benefit. The mechanism by which quiescent fibroblasts are converted into CAFs is unclear. The present study identifies a set of 3 miRNAs that reprogram normal fibroblasts to CAFs. These miRNAs may represent novel therapeutic targets in the tumor microenvironment. ©2012 AACR.
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            Ovarian cancer-associated fibroblasts contribute to epithelial ovarian carcinoma metastasis by promoting angiogenesis, lymphangiogenesis and tumor cell invasion.

            Yuan Zhang, Huijuan Tang, Jing Cai … (2011)
            Cancer-associated fibroblasts (CAFs) are thought to play an essential role in cancer initiation and development. However, little research has been done to evaluate the role of CAFs in epithelial ovarian cancer (EOC) development. To address this issue, ninety-one specimens were immunostained with α-smooth muscle actin (α-SMA) and fibroblast activation protein (FAP) antibodies to quantify CAFs, and antibodies D2-40 and CD34 to evaluate the lymphatic vessel density (LVD) and microvessel density (MVD) of the lesions. We found there were no α-SMA or FAP positive fibroblasts in normal ovary tissues. More CAFs were found in EOC than in borderline tumors and benign tumors (P<0.01). Abundant CAFs in EOC were associated with advanced-stage disease (P=0.002), the occurrence of lymph node metastases (P=0.02) and omentum metastases (P<0.0001), and increased LVD (P=0.002) and MVD (P=0.0004). CAFs isolated from EOC tissues induced more cancer cells to invade (P=0.003) and migrate (P=0.005) compared with normal fibroblasts (NFs) isolated from normal ovary tissues in vitro. Our data indicate that CAFs play a vital role in ovarian cancer progression and metastasis. Targeting CAFs as a therapeutic strategy against ovarian cancer is an intriguing concept that needs further study. Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.
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              Cancer associated fibroblasts express pro-inflammatory factors in human breast and ovarian tumors.

              Neta Erez, Sarah Glanz, Yael Raz … (2013)
              Inflammation has been established in recent years as a hallmark of cancer. Cancer Associated Fibroblasts (CAFs) support tumorigenesis by stimulating angiogenesis, cancer cell proliferation and invasion. We previously demonstrated that CAFs also mediate tumor-enhancing inflammation in a mouse model of skin carcinoma. Breast and ovarian carcinomas are amongst the leading causes of cancer-related mortality in women and cancer-related inflammation is linked with both these tumor types. However, the role of CAFs in mediating inflammation in these malignancies remains obscure. Here we show that CAFs in human breast and ovarian tumors express high levels of the pro-inflammatory factors IL-6, COX-2 and CXCL1, previously identified to be part of a CAF pro-inflammatory gene signature. Moreover, we show that both pro-inflammatory signaling by CAFs and leukocyte infiltration of tumors are enhanced in invasive ductal carcinoma as compared with ductal carcinoma in situ. The pro-inflammatory genes expressed by CAFs are known NF-κB targets and we show that NF-κB is up-regulated in breast and ovarian CAFs. Our data imply that CAFs mediate tumor-promoting inflammation in human breast and ovarian tumors and thus may be an attractive target for stromal-directed therapeutics. Copyright © 2013 Elsevier Inc. All rights reserved.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Onco Targets Ther
                Journal ID (iso-abbrev): Onco Targets Ther
                Journal ID (publisher-id): OTT
                Journal ID (pmc): ott
                Title: OncoTargets and therapy
                Publisher: Dove
                ISSN (Electronic): 1178-6930
                Publication date (Electronic): 11 April 2019
                Publication date Collection: 2019
                Volume: 12
                Pages: 2789-2798
                Affiliations
                [1 ]Department of Obstetrics and Gynecology, The Fifth People’s Hospital of Shanghai, Fudan University , Shanghai, People’s Republic of China
                [2 ]Department of Obstetrics and Gynecology, Zhongshan Hospital, Fudan University , Shanghai, People’s Republic of China
                [3 ]Obstetrics and Gynecology Hospital of Fudan University , Shanghai, People’s Republic of China
                Author notes
                Correspondence: Lina YangDepartment of Obstetrics and Gynecology, The Fifth People’s Hospital of Shanghai, Fudan University , 801 Heqing Road, Shanghai200240, People’s Republic of ChinaTel +86 213 490 4800Email linayang12@ 123456fudan.edu.cn
                Yaping ChenDepartment of Obstetrics and Gynecology, The Fifth People’s Hospital of Shanghai, Fudan University , 801 Heqing Road, Shanghai200240, People’s Republic of ChinaTel +86 212 428 9559Email chenyaping@ 1234565thhospital.com
                [*]

                These authors contributed equally to this work

                Article
                Publisher ID: 196150
                DOI: 10.2147/OTT.S196150
                PMC ID: 6489642
                PubMed ID: 31114228
                SO-VID: fdd35de1-b7b5-4fcf-b3fc-a6ce08fedb99
                Copyright © © 2019 Yang et al.
                License:

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                History
                Date received : 27 November 2018
                Date accepted : 06 March 2019
                Page count
                Figures: 4, References: 23, Pages: 10
                Categories
                Subject: Original Research

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: stc1,tumor microenvironment,cafs,emt,metastasis
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: stc1, tumor microenvironment, cafs, emt, metastasis

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