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Increasing evidence suggests that the renin-angiotensin system (RAS) plays an important role in tumorigenesis. The interaction between Angiotensin II (AngII) and angiotensin type 1 receptor (AT1R) may have a pivotal role in hepatocellular carcinoma (HCC) and therefore, AT1R blocker and angiotensin I-converting enzyme (ACE) inhibitors may have therapeutic potential in the treatment of hepatic cancer. Although the involvement of AT1R has been well explored, the role of the angiotensin II Type 2 receptor (AT2R) in HCC progression remains poorly understood. Thus, the aim of this study was to explore the effects of AT2R overexpression on HCC cells in vitro and in mouse models of human HCC. An AT2R recombinant adenoviral vector (Ad-G-AT2R-EGFP) was transduced into HCC cell lines and orthotopic tumor grafts. The results indicate that the high dose of Ad-G-AT2R-EGFP–induced overexpression of AT2R in transduced HCC cell lines produced apoptosis. AT2R overexpression in SMMC7721 cells inhibited cell proliferation with a significant reduction of S-phase cells and an enrichment of G1-phase cells through changing expression of CDK4 and cyclinD1. The data also indicate that overexpression of AT2R led to apoptosis via cell death signaling pathway that is dependent on activation of p38 MAPK, pJNK, caspase-8 and caspase-3 and inactivation of pp42/44 MAPK (Erk1/2). Finally, we demonstrated that moderately increasing AT2R expression could increase the growth of HCC tumors and the proliferation of HCC cells in vivo. Our findings suggest that AT2R overexpression regulates proliferation of hepatocellular carcinoma cells in vitro and in vivo, and the precise mechanisms of this phenomenon are yet to be fully determined.

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Migratory behaviour in insects correlates with reproductive development in females, and migration often occurs during the pre‐reproductive stage of adults. The relationship between ovarian development and population status of the white‐backed planthopper Sogatella furcifera (Horváth) and the brown planthopper Nilaparvata lugens (Stål) was evaluated. Females of both species were captured in rice fields and light traps and then dissected in double‐season rice‐farming regions of southern China. The ovarian development of S. furcifera and N. lugens was divided into five levels, following previous studies. The population statuses of both species were examined based on the ovarian development of female adults caught in rice paddies. The ovarian development in N. lugens females caught in light traps mostly ranged from level I to level II, whereas that in S. furcifera females caught in light traps mostly ranged from level I to level III. During peak immigration, ovarian development in N. lugens females was mainly at level II, whereas that in S. furcifera females was mainly at level II and sporadically at level III. During peak emigration, both S. furcifera and N. lugens showed level I ovarian development. The temporal dynamics of ovarian development in light trap catches revealed that (i) significant emigration and partial immigration periods occur in S. furcifera, with ovarian development mainly at level I and sporadically from level II to level III and (ii) numerous immigrants of N. lugens were detected during sedentary and local breeding periods. The temporal dynamics of ovarian development provides more information than does the paddy population. Thus, this study proposes another method for pest forecasting, which is more precise and efficient than conventional forecasting methods such as light trap catching and monitoring population dynamics in rice fields.

Purpose To evaluate the role of DiGeorge Critical Region 8 (DGCR8), a key component of miRNA biogenesis pathway in ovarian cancer. Methods The expression of DGCR8 in ovarian cancer was detected by immunostaining and DGCR8 knockdown in ovarian cancer cells was achieved using lentiviral shRNA. Differential expression of miRNAs was determined using Nanostring miRNA arrays and validated by real-time RT-PCR. Results DGCR8 was highly expressed in ovarian cancer. Knockdown of DGCR8 expression inhibits cell proliferation, migration, and invasion, as well as sensitizes cells to apoptosis induced by the chemotherapeutic drug cisplatin. Cellular survival pathways including ERK1/2 mitogen-activated protein kinase and phosphatidylinositol 3-kinase/AKT were attenuated in DGCR8 knockdown cells. DGCR8 knockdown resulting in dysregulated miRNA gene expression. miR-27b was identified as the most highly down-regulated miRNA in DGCR8 knockdown cells and promoted cell proliferation in ovarian cancer cells. Conclusions DGCR8 functions as an oncogene in ovarian cancer, which is in part mediated by miR-27b.