[1] Bray F, Ferlay J, Soerjomataram I et al. Global cancer statistics 2018: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA Cancer J Clin. 68(6), 394-424(2018).
[2] Chen W, Zheng R, Baade PD et al. Cancer statistics in China, 2015. CA Cancer J Clin. 66(2), 115-32 (2016).
[3] Ajani JA, D'Amico TA, Almhanna K et al. National comprehensive cancer network. Esophageal and esophagogastric junction cancers, version1. 2015. J Natl Compr Canc Netw. 13(2), 194-227 (2015).
[4] Delgado-Bellido D, Fernández-Cortés M, Rodríguez MI et al. VE-cadherin promotes vasculogenic mimicry by modulating kaiso-dependent gene expression. Cell Death Differ. 26(2), 348-61 (2019).
[5] Zhang J, Zhang G, Hu P et al. Vasculogenic mimicry is associated with increased tumor-infiltrating neutrophil and poor outcome in esophageal squamous cell carcinoma. Onco Targets Ther. 10, 2923-30 (2017).
[6] Cappelli HC, Kanugula AK, Adapala RK et al. Mechanosensitive TRPV4 channels stabilize VE-cadherin junctions to regulate tumor vascular integrity and metastasis. Cancer Lett. 442, 15-20 (2019).
[7] Paatero I, Sauteur L, Lee M. Junction-based lamellipodia drive endothelial cell rearrangements in vivo via a VE-cadherin-F-actin based oscillatory cell-cell interaction. Nat Commun. 9(1), 3545 (2018).
[8] Yeo C, Lee HJ, Lee EO. Serum promotes vasculogenic mimicry through the EphA2/VE-cadherin/AKT pathway in PC-3 human prostate cancer cells. Life Sci. 221, 267-73 (2019).
[9] Delgado-Bellido D, Fernández-Cortés M, Rodríguez MI et al. VE-cadherin promotes vasculogenic mimicry by modulating kaiso-dependent gene expression. Cell Death Differ. 26(2), 348-61 (2019).
[10] Gubbay J, Collignon J, Koopman P et al. A gene mapping to the sex-determining region of the mouse Y chromosome is a member of a novel family of embryonically expressed genes. Nature. 346(6281), 245-50 (1990).
[11] Lovell-Badge R. The early history of the Sox genes. Int J Biochem Cell Biol. 42(3), 378-80 (2010).
[12] Hou L, Srivastava Y, Jauch R. Molecular basis for the genome engagement by Sox proteins. Semin Cell Dev Biol. 63, 2-12 (2017).
[13] Kamachi Y, Kondoh H. Sox proteins: regulators of cell fate specification and differentiation. Development. 140(20), 4129-44 (2013).
[14] Lefebvre V, Dumitriu B, Penzo-Méndez A et al. Control of cell fate and differentiation by Sry-related high-mobility-group box (Sox) transcription factors. Int J Biochem Cell Biol. 39(12), 2195-214 (2007).
[15] Kanai Y, Kanai-Azuma M, Noce T et al. Identification of two Sox17 messenger RNA isoforms, with and without the high mobility group box region, and their differential expression in mouse spermatogenesis. J Cell Biol. 133(3), 667-81 (1996).
[16] Zhang Y, Bao W, Wang K et al. SOX17 is a tumor suppressor in endometrial cancer. Oncotarget. 7(46), 76036-46 (2016).
[17] Sinner D, Kordich JJ, Spence JR et al. Sox17 and Sox4 differentially regulate beta-catenin/T-cell factor activity and proliferation of colon carcinoma cells. Mol Cell Biol. 27(22), 7802-15 (2007).
[18] Zhang W, Glöckner SC, Guo M et al. Epigenetic inactivation of the canonical Wnt antagonist SRY-box containing gene 17 in colorectal cancer. Cancer Res. 68(8), 2764-72 (2008).
[19] Yin D, Jia Y, Yu Y et al. SOX17 methylation inhibits its antagonism of Wnt signaling pathway in lung cancer. Discov Med. 14(74), 33-40 (2012).
[20] Jia Y, Yang Y, Liu S et al. SOX17 antagonizes WNT/β-catenin signaling pathway in hepatocellular carcinoma. Epigenetics. 5(8), 743-9 (2010).
[21] Moreno CS. The Sex-determining region Y-box 4 and homeobox C6 transcriptional networks in prostate cancer progression: crosstalk with the Wnt, Notch, and PI3K pathways. Am J Pathol. 176(2), 518-27 (2010).
[22] Rhodes DR, Yu J, Shanker K et al. Large-scale meta-analysis of cancer microarray data identifies common transcriptional profiles of neoplastic transformation and progression. Proc Natl Acad Sci USA. 101(25), 9309-14 (2004).
[23] Aaboe M, Birkenkamp-Demtroder K, Wiuf C et al. SOX4 expression in bladder carcinoma: clinical aspects and in vitro functional characterization. Cancer Res. 66(7), 3434-42(2006).
[24] Qin Y, Zhao W, Cheng L et al. Clinical significance of vasculogenic mimicry, vascular endothelial cadherin and SOX4 in patients with esophageal squamous cell carcinoma. Int J Clin Exp Pathol. 12(7), 2462-73 (2019).
[25] Xia J, Cheng L, Mei C, et al. Genistein inhibits cell growth and invasion through regulation of miR-27a in pancreatic cancer cells. Curr Pharm Des. 20(33), 5348-53 (2014).
[26] Yang Q, Huang J, Wu Q, et al. Acquisition of epithelial-mesenchymal transition is associated with Skp2 expression in paclitaxel-resistant breast cancer cells. Br J Cancer. 110(8), 1958-67 (2014).
[27] Tang NN, Zhu H, Zhang HJ et al. HIF-1α induces VE-cadherin expression and modulates vasculogenic mimicry in esophageal carcinoma cells. World J Gastroenterol. 20(47), 17894-904 (2014).
[28] Cappelli HC, Kanugula AK, Adapala RK et al. Mechanosensitive TRPV4 channels stabilize VE-cadherin junctions to regulate tumor vascular integrity and metastasis. Cancer Lett. 442, 15-20 (2019).
[29] Zhang J, Qiao L, Liang N et al. Vasculogenic mimicry and tumor metastasis. J BUON. 21(3), 533-41 (2016).
[30] Hendrix MJ, Seftor EA, Meltzer PS et al. Expression and functional significance of VE-cadherin in aggressive human melanoma cells: role in vasculogenic mimicry. Proc Natl Acad Sci USA. 98(14), 8018-23(2001).
[31] Heinolainen K, Karaman S, D'Amico G et al. VEGFR3 Modulates Vascular Permeability by Controlling VEGF/VEGFR2 Signaling. Circ Res. 120(9), 1414-25 (2017).
[32] Han H, Du L, Cao Z et al. Triptonide potently suppresses pancreatic cancer cell-mediated vasculogenic mimicry by inhibiting expression of VE-cadherin and chemokine ligand 2 genes. Eur J Pharmacol. 818, 593-603 (2018).
[33] Kuo IY, Wu CC, Chang JM et al. Low SOX17 expression is a prognostic factor and drives transcriptional dysregulation and esophageal cancer progression. Int J Cancer. 135(3), 563-73 (2014).
[34] Zhang W, Glöckner SC, Guo M et al. Epigenetic inactivation of the canonical Wnt antagonist SRY-box containing gene 17 in colorectal cancer. Cancer Res. 68(8), 2764-72 (2008).
[35] Kuo IY, Huang YL, Lin CY et al. SOX17 overexpression sensitizes chemoradiation response in esophageal cancer by transcriptional down-regulation of DNA repair and damage response genes. J Biomed Sci. 26(1), 20 (2019).
[36] Schilham MW, Oosterwegel MA, Moerer P et al. Defects in cardiac outflow tract formation and pro-B-lymphocyte expansion in mice lacking Sox-4. Nature. 380(6576), 711-4 (1996).
[37] Wu Z, Yu B, Jiang L. MiR-212-3p mediates apoptosis and invasion of esophageal squamous cell carcinoma through inhibition of the Wnt/β-catenin signaling pathway by targeting SOX4. J Thorac Dis. 12(8), 4357-67 (2020).
[38] Hulin JA, Tommasi S, Elliot D et al. Small molecule inhibition of DDAH1 significantly attenuates triple negative breast cancer cell vasculogenic mimicry in vitro. Biomed Pharmacother. 111, 602-612 (2019).
[39] Bai J, Yeh S, Qiu X et al. TR4 nuclear receptor promotes clear cell renal cell carcinoma (ccRCC) vasculogenic mimicry (VM) formation and metastasis via altering the miR490-3p/vimentin signals. Oncogene. 37(44), 5901-12 (2018).
[40] Kawahara R, Niwa Y, Simizu S. Integrin β1 is an essential factor in vasculogenic mimicry of human cancer cells. Cancer Sci. 109(8), 2490-6 (2018).
[41] Ge H, Luo H. Overview of advances in vasculogenic mimicry - a potential target for tumor therapy. Cancer Manag Res. 10, 2429-37 (2018).