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Human hepatocellular carcinoma (HCC) is the fifth most common cancer worldwide with a poor prognosis of limited survival. The role of regulatory B cell (Breg), a new important B cell subset, in HCC progression remains unclear. We firstly found that the percentage of B cells at tumor margin was significantly higher than that in tumor and non-tumor regions. Especially, increased intrahepatic B cells at tumor margin were positively associated with tumor invasive features and more tumor recurrence. Besides, HCC patients had a significantly higher percentage of circulating Bregs than healthy people. Increased circulating Bregs were correlated with advanced tumor staging, tumor multiplicity and venous infiltration. Next, we firstly revealed that human Bregs promoted HCC tumor growth independent of Tregs in SCID mice. The migration of Bregs from blood into tumor was also confirmed in mice. Finally, we further explored the molecular mechanism of Bregs promoting proliferation and migration of HCC cells in vitro . Bregs promoted HCC growth and invasiveness by directly interacting with liver cancer cells through the CD40/CD154 signaling pathway. [ABSTRACT FROM AUTHOR]

Abstract: Oral squamous cell carcinoma (OSCC) is associated with a high potential of tumor recurrence and metastasis, leading to poor prognosis. Cell motility is an important factor in the progression and metastasis of cancers. Recently, Fascin has been linked to tumor progression by induction of cell motility. However, the precise roles of Fascin in OSCC have not been elucidated clearly. The aim of this study was to analyze the roles of Fascin in OSCC progression using OSCC clinical samples. We demonstrated that Fascin over-expression was found in OSCC clinical samples and its expression was significantly associated with nodal metastasis (p =0.027), tumor recurrence (p <0.001) and poor patients’ overall survival (p =0.013). Consistently, Fascin proteins were detected in all OSCC cell lines with the expression level corresponding to the invasion ability. To specifically investigate the mechanism of Fascin in OSCC, we examined the E-cadherin expression in the same set of OSCC specimens. Fascin was negatively correlated with E-cadherin expression (p =0.018, r =−0.513). In conclusion, our findings suggested that Fascin over-expression might enhance OSCC aggressiveness, possibly by interacting with E-cadherin expression. [Copyright &y& Elsevier]