Unlike other members of the VEGF family, the function of VEGF-B in tumor progression remains to be elucidated. Thus, the present study aimed to determine the function of VEGF-B in human choriocarcinoma cells by investigating its detailed effects and molecular mechanisms. VEGF-B and aryl hydrocarbon receptor (AhR) expression were evaluated by reverse transcription-quantitative PCR analysis and western blot analysis in JEG-3 cells and choriocarcinoma stem-like cells (CSLCs) and their proliferation, migration, and invasion after the transfection of short hairpin RNA VEGF-B, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD; AhR agonist) treatment or StemRegenin 1 (SR1; AhR antagonist) treatment were examined by cell proliferation assay, wound healing assay and Transwell assay. In addition, luciferase reporter analysis and bioinformatics data mining were used to investigate the association between VEGF-B and AhR. Upregulation of VEGF-B and AhR expression was observed in CSLCs. Following VEGF-B knockdown or SR1 treatment, the proliferative, migratory, and invasive abilities of CSLCs were significantly decreased, contrary to the findings after TCDD treatment. It was also found that AhR enhanced VEGF-B transcriptional activity by binding to the relative promoter region. These observations indicated that VEGF-B may be an oncogene that promotes choriocarcinoma cell migration and invasion targeted by AhR. Therefore, targeting VEGF-B may provide a novel therapeutic opportunity for choriocarcinoma.

Background: To establish a functional monoclonal antibody library using Human Uterine Sarcoma Stem Cell-Like Cells (HUSSLCs) to screen and identify functional monoclonal antibodies that can recognize and inhibit HUSSLCs. Methods: B lymphocytes in proliferative state were prepared by using the second generation CD133+spheroid cells of SK-UT-1 cell line, i.e. HUSSLCs, as antigens; Spheroid formation, agar colony formation, wound healing, flow cytometry, and Western blotting were adopted to detect the effect of monoclonal antibodies with varied dilution ratios on HUSSLCs spheroid formation, agar colony formation, cell migration, CD133 expression, and expression of CD44, ABCG2, Bmi1, Nanog, Oct4 and ALDH1. Results: Myeloma cells of SP2/0 cell line can achieve 85% degrees of fusion and results of 1-2F monoclonal cell supernatants with different dilution ratios reduced HUSSLCs spheroid formation rate, agar colony formation rate, cell migration rate, CD133 positive cell expression and protein expression levels of CD44, ABCG2, Bmi1, Nanog, Oct4, and ALDH1 in concentration-dependent manner (P <0.05). Conclusion: The antibody valence produced by HUSSLCs-immunized mice reached the requirement for preparation of monoclonal antibody. Anti-HUSSLCs monoclonal antibodies feature functions of inhibiting the self-renewal, unrestricted proliferation, migration, invasion and multidrug resistance of HUSSLCs and functions characterized by tumor stem cells. Key words: uterine leiomyosarcoma; tumor stem cell; monoclonal antibody; self-renewal ability; infinite multiplication; drug resistance