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FSTL1 Promotes Metastasis and Chemoresistance in Esophageal Squamous Cell Carcinoma Through Nfκb-BMP Signaling Crosstalk

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FSTL1 Promotes Metastasis and Chemoresistance in Esophageal Squamous Cell Carcinoma Through Nfκb-BMP Signaling Crosstalk Author Manuscript Published OnlineFirst on September 7, 2017; DOI: 10.1158/0008-5472.CAN-17-1411 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. FSTL1 promotes metastasis and chemoresistance in esophageal squamous cell carcinoma through NFκB-BMP signaling crosstalk Marco Chi-Chung Lau1#, Kai Yu Ng1#, Tin Lok Wong1, Man Tong1, Terence K. Lee5, Xiao-Yan Ming2, Simon Law3, Nikki P. Lee3, Annie L. Cheung1, Yan-Ru Qin6, Kwok Wah Chan4, Wen Ning7, Xin-Yuan Guan2, Stephanie Ma1 1School of Biomedical Sciences, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong; Departments of 2Clinical Oncology, 3Surgery and 4Pathology, Li Ka Shing Faculty of Medicine, Queen Mary Hospital, The University of Hong Kong, Hong Kong; 5Department of Applied Biology and Chemical Technology, Hong Kong Polytechnic University, Hong Kong; 6Department of Clinical Oncology, First Affiliated Hospital, Zhengzhou University, Zhengzhou, China and 7Department of Genetics and Cell Biology, College of Life Sciences, Nankai University, Tianjin, China #Equal contribution Corresponding author: Dr. Stephanie Ma, PhD, School of Biomedical Sciences, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Room 47, 1/F, Laboratory Block, Faculty of Medicine Building, 21 Sassoon Road, Pok Fu Lam, Hong Kong. Phone: (852) 3917 9238; Fax: (852) 2817 0857; E-mail: [email protected]. Grant support: This study was supported by funding from the Research Grants Council of Hong Kong - Collaborative Research Fund (C7038-14G) to XY Guan and S Ma. Short title: FSTL1-mediated NFκB and BMP pathway deregulation in ESCC Keywords: FSTL1, NFκB, SMAD, BMP, chemoresistance, metastasis, ESCC 1 Downloaded from cancerres.aacrjournals.org on September 27, 2021. © 2017 American Association for Cancer Research. Author Manuscript Published OnlineFirst on September 7, 2017; DOI: 10.1158/0008-5472.CAN-17-1411 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Abstract Esophageal squamous cell carcinoma (ESCC) has a generally poor prognosis and molecular markers to improve early detection and predict outcomes are greatly needed. Here we report that the BMP-binding follistatin-like protein FSTL1 is overexpressed in ESCCs where it correlates with poor overall survival. Genetic amplification of FSTL1 or chromosome 3q where it is located occurred frequently in ESCC, where FSTL1 copy number correlated positively with higher FSTL1 protein expression. Elevating FSTL1 levels by various means was sufficient to drive ESCC cell proliferation, clonogenicity, migration, invasion, self-renewal and cisplatin resistance in vitro and tumorigenicity and distant metastasis in vivo. Conversely, FSTL1 attenution by shRNA or neutralizing antibody elicited the opposite effects in ESCC cells. mRNA profiling analyses suggested that FSTL1 drives ESCC oncogenesis and metastasis through various pathways with deregulation of NFκB and BMP signaling figuring prominently. Crosstalk between the NFκB and BMP pathways was evidenced by functional rescue experiments using inhibitors of NFκB and TLR4. Our results establish the significance of FSTL1 in driving oncogenesis and metastasis in ESCC by coordinate NFκB and BMP pathway control, with implications for its potential use as a diagnostic or prognostic biomarker and a candidate therapeutic target in this disease setting. 2 Downloaded from cancerres.aacrjournals.org on September 27, 2021. © 2017 American Association for Cancer Research. Author Manuscript Published OnlineFirst on September 7, 2017; DOI: 10.1158/0008-5472.CAN-17-1411 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Introduction Esophageal squamous cell carcinoma (ESCC) is the most common histologic subtype of esophageal cancer. The disease is ranked as the eighth most common cancer and the sixth leading cause of cancer mortalities worldwide, with a dismal prognosis (1). The overall prognosis for ESCC is poor due to late presentation, high incidences of tumor recurrence and metastasis, as well as the ability of the tumor to acquire chemoresistance. A better understanding of the recurrently altered genomic and molecular profiles involved in ESCC development, progression and therapy resistance should aid in the identification of novel targets and the development of new therapies for the more effective clinical management of this disease. To date, there is no effective biomarker for the diagnosis or prognosis of ESCC, nor a good targeted therapeutic drug for the adjuvant treatment of the disease. To identify better molecular markers for early detection and therapeutic targeting, our lab has previously performed transcriptome sequencing on three pairs of patient-derived ESCC samples and their adjacent non-tumor tissue counterparts (2) and successfully identified a number of commonly and differentially expressed genes at a global level. Based on this profiling data, we have identified PTK6 and RAB25 as novel tumor and metastasis suppressors of ESCC (2-3), CD90 to represent a novel ESCC cancer stem cell subpopulation (4), and NRP2 as a novel oncogene in ESCC (5). However, our knowledge of the exact cellular and molecular mechanisms leading to ESCC is incomplete. Through data mining of our transcriptome sequencing data, we found the transmembrane glycoprotein follistatin-like 1 (FSTL1), belonging to the BM-40/SPARC/osteonectin family (6), to be commonly overexpressed in all three ESCC samples compared with its corresponding non- tumor counterparts (p<0.005). FSTL1 became an obvious candidate gene of interest as it is located on chromosome 3q13.33, which has previously been reported to be a chromosomal amplification hotspot in ESCC (7-9). FSTL1 is involved in the development of different organogenesis including early development of the lung, ureter, central nervous system and skeleton (10-14). FSTL1 has also been implicated to act as an auto-antigen associated with rheumatoid arthritis and to elicit a cardioprotective role in various cardiovascular diseases (15-18). The link between FSTL1 and rheumatoid arthritis is particularly strong, where Tanaka et al. first cloned the gene from synovial 3 Downloaded from cancerres.aacrjournals.org on September 27, 2021. © 2017 American Association for Cancer Research. Author Manuscript Published OnlineFirst on September 7, 2017; DOI: 10.1158/0008-5472.CAN-17-1411 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. tissues of rheumatoid arthritis patients in 1998 and found FSTL1 to be detected in the sera and synovial fluid of patients suffering from the disease (19). Mechanistically, FSTL1 have been shown to regulate the TGF-β/BMP pathway and as a result leading to blockage of erythroid cell differentiation and subsequent apoptosis (20), as well as abnormal skeletal and lung organogenesis in mice (11-12). In addition to TGF-β/BMP, FSTL1 has also been shown to activate NFκB, via both canonical and non-canonical means, to trigger inflammation in osteoarthritis (21) and obesity (22). Only a small number of studies have reported on the role of FSTL1 in cancer, and many of them with contradictory organ-specific roles. FSTL1 has been shown to negatively regulate the migratory and invasive abilities of ovarian, endometrial, renal, lung and nasopharyngeal cancers (23-26). However, FSTL1 was found to be overexpressed in astrocytic brain tumors (27) and also to enhance the metastasis of cancer cells in breast prostate, skin and pancreatic cancers (28-29). A recent study have also found knockdown of FSTL1 to induce mitotic cell death and BIM up-regulation in non-small cell lung carcinoma cells (30). However, to date, the clinical significance and functional role of endogenous and secretory FSTL1 and the molecular mechanism by which it drives ESCC pathogenesis has not been reported. The link between FSTL1 and the crosstalk between BMP and NFκB pathways have also not been implicated in cancer previously. In this present study, we found both endogenous and secretory FSTL1 to be markedly up- regulated in ESCC tissue and serum samples and that their overexpression was significantly correlated with worst survival of ESCC patients. FSTL1 copy number positively correlated with high FSTL1 expression in both ESCC cell lines and clinical samples, suggesting that FSTL1 gene and/or chromosome 3q amplification contributes, at least in part, to the preferential up- regulation of FSTL1 in ESCC. Overexpression of FSTL1 provoked, whereas silencing FSTL1 abrogated proliferation, clonogenicity, migration, invasion, self-renewal and cisplatin resistance in ESCC in vitro as well as tumorigenicity and distant metastasis in vivo. Co-culture of FSTL1- containing conditioned medium or recombinant FSTL1 in low FSTL1-expressing ESCC cells enhanced the cells’ ability to migrate and invade in vitro as well as form tumors in vivo; whereas treatment of high FSTL1 expressing ESCC cells with a FSTL1 neutralizing antibody resulted in decreased ESCC metastasis. Mechanistically, FSTL1 modulated ESCC tumorigenicity and metastasis through de-regulation of both NFκB and BMP signaling pathways crosstalk, as evidenced by mRNA profiling of ESCC cells with or without FSTL1 stably overexpressed, coupled 4 Downloaded from cancerres.aacrjournals.org on September 27, 2021. © 2017 American Association for Cancer Research. Author Manuscript Published OnlineFirst on September 7, 2017; DOI: 10.1158/0008-5472.CAN-17-1411 Author
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