It is largely recognized that fibroblast activation protein (FAP) is expressed in cancer-associated fibroblasts (CAFs) of many human carcinomas. Furthermore, FAP was recently also reported to be expressed in carcinoma cells of the breast, stomach, pancreatic ductal adenocarcinoma, colorectum, and uterine cervix. The carcinoma cell expression pattern of FAP has been described in several types of cancers, but the role of FAP in oral squamous cell carcinoma (OSCC) is unknown. The role of endogenous FAP in epithelium-derived tumors and molecular mechanisms has also not been reported. In this study, FAP was found to be expressed in carcinoma cells of OSCC and was upregulated in OSCC tissue samples compared with benign tissue samples using immunohistochemistry. In addition, its expression level was closely correlated with overall survival of patients with OSCC. Silencing FAP inhibited the growth and metastasis of OSCC cells in vitro and in vivo. Mechanistically, knockdown of FAP inactivated PTEN/PI3K/AKT and Ras-ERK and its downstream signaling regulating proliferation, migration, and invasion in OSCC cells, as the inhibitory effects of FAP on the proliferation and metastasis could be rescued by PTEN silencing. Our study suggests that FAP acts as an oncogene and may be a potential therapeutic target for patients with OSCC.

Connective tissue growth factor (CTGF) has different roles in different types of cancer. However, the involvement and molecular basis of CTGF in tumor progression and prognosis of human nasopharyngeal carcinoma (NPC) have almost never been reported. In this study, we observed that downregulated CTGF expression was significantly associated with NPC progression and poor prognosis. Knockdown of CTGF markedly elevated the ability of cell proliferation in vivo and in vitro. Subsequently, we discovered that the reduction of CTGF increased the expression of miR-18b, an oncomir-promoting cell proliferation. Further, we discovered that attenuated CTGF-mediated upregulation of miR-18b was dependent on the increased binding of transcription factors Jun proto-oncogene (C-Jun) and v-Myc myelocytomatosis viral oncogene homolog (C-Myc) to miR-18b promoter region via phosphoinositide 3-kinase (PI3K)/AKT pathway. Finally, we further found that miR-18b directly suppressed the expression of CTGF in NPC. In clinical fresh specimens, miR-18b was widely overexpressed and inversely correlated with CTGF expression in NPC. Our studies are the first to demonstrate that reduced CTGF as an unfavorable prognosis factor mediates the activation of miR-18b, an oncomir directly suppresses CTGF expression, by PI3K/AKT/C-Jun and C-Myc and promotes cell growth of NPC.

The aim of this study was to compare the efficacy of lamivudine vs entecavir in the prevention of hepatitis B virus (HBV) reactivation in HBV surface Ag (HBsAg)-positive patients undergoing allogeneic hematopoietic stem cell transplantation (allo-HSCT). A total of 216 consecutive patients were enrolled and retrospectively reviewed. Of these patients, 119 received lamivudine and 97 received entecavir. The median treatment duration to complete virological response in patients with baseline HBV-DNA levels 410 5 copies/mL was 2.0 months in the entecavir group, significantly shorter than that of the lamivudine group. After a median follow-up of 24 months post transplantation, the cumulative incidence rates of HBV reactivation at 6, 12 and 24 months following transplantation were 3.0%, 7.0% and 24.0% in the lamivudine group, and 0%, 0% and 2.0% in the entecavir group, respectively. In addition, entecavir treatment was associated with lower cumulative incidence rates of severe hepatitis caused by HBV reactivation. Mutations leading to drug resistance were detected in 25 patients in the lamivudine group and in only one patient in the entecavir group. Our data indicate that compared with lamivudine, entecavir has more potent antiviral efficacy and may be a better choice for prophylaxis of HBV reactivation in HBsAg-positive allo-HSCT recipients.