The histidine-rich calcium binding protein (HRC) is a regulator of Ca2+-homeostasis. Herein, we found that HRC was frequently upregulated in human hepatocellular carcinoma (HCC) tissues, and its expression was correlated with tumor size and metastasis. Moreover, HRC expression was positively related to the metastatic potential of HCC cell lines. Knockdown of HRC suppressed cell invasion and migration in vitro, whereas ectopic expression of HRC resulted in increased cell invasion and migration in vitro and intrahepatic and lung metastasis in vivo. Interestingly, the pro-invasion and pro-migration effects of HRC were associated with focal adhesion turnover, which was a consequence of FAK phosphorylation. Further experiments showed that HRC induced phospho-FAK, focal adhesion turnover and cell migration through Ca2+/CaM singaling. We found that HRC increased [Ca2+]i by inhibiting the expression of SERCA2. In addition, upregulation of HRC in HCC was attributed to SATB1, which is known to promote HCC metastasis. Ectopic expression of SATB1 enhanced HRC gene transcription by activating AP-1 in mainly a JNK-dependent manner. Our findings highlight HRC as a potential therapeutic target for HCC treatment.

The demand for greenhouse gas measurement has increased dramatically due to global warming. A 1.57-μm airborne double-pulse integrated-path differential absorption (IPDA) light detection and ranging (LIDAR) system for CO2 concentration measurement was developed. The airborne field experiments of this IPDA LIDAR system were conducted at a flight altitude of approximately 7 km, and the weak echo signal of the ocean area was successfully received. The matched filter algorithm was applied to the retrieval of the weak signals, and the pulse integration method was used to improve the signal-to-noise ratio. The inversion results of the CO2 column-averaged dry-air mixing ratio (XCO2) by the scheme of averaging after log (AVD) and the scheme of averaging signals before log were compared. The AVD method was found more effective for the experiment. The long-term correlation between the changing trends of XCO2 retrieved by the IPDA LIDAR system and CO2 dry-air volume mixing ratio measured by the in-situ instrument reached 92%. In the steady stage of the open area (30 km away from the coast), which is almost unaffected by the residential areas, the mean value of XCO2 retrieved by the IPDA LIDAR system was 414.69 ppm, with the standard deviation being 1.02 ppm. Compared with the CO2 concentration measured by the in-situ instrument in the same period, bias was 1.30 ppm. The flight path passed across the ocean, residential, and mountainous areas, with the mean value of XCO2 of the three areas being 419.35, 429.29, and 422.52 ppm, respectively. The gradient of the residential and ocean areas was 9.94 ppm, with that of the residential and mountainous areas being 6.77 ppm. Obvious gradients were found in different regions.

Elevated expression of CXCL9 has been shown to involve in the infiltration of inflammatory cells and liver damage after Hepatitis B virus (HBV) infection. However, whether and by what underlying mechanism does CXCL9 play a role in HBV infection associated hepatocellular carcinoma (HCC) invasion ability remain unclear. In this study, human HCC as well as adjacent noncancerous tissues, together with three kinds of liver cancer cell lines were investigated to clarify the possible involvement of CXCL9 in the regulation of HCC invasion and metastasis. Invasion ability of liver cancer cells were evaluated by transwell assays and it is enhanced after co-cultured with recombined human CXCL9 (rhCXCL9). As a trigger of Rac GTPase signaling after G protein-coupled receptors (GPCR) activated by CXCL9, Phosphatidylinositol-3, 4, 5-trisphosphate RAC Exchanger 2 (PREX2) mRNA expression of the liver cancer cell lines was elevated after co-cultured with rhCXCL9. Moreover, the mRNA level of PREX2 in HCC tissues was significantly higher than those in adjacent noncancerous tissues. Besides, the mRNA levels of PREX2 were positively correlated with the poor differentiation, portal vein invasion, metastasis and qualitative HbsAg results in 45 pairs of HCC specimens. Similarly, PREX2 mRNA was higher in three liver cancer cell lines when compared with the normal liver cell line whereas knocked down of PREX2 by small interference RNA (PREX2-siRNA) reduced the invasion ability of liver cancer cells in transwell assays. Overall, our results suggested CXCL9 was involved in the invasion ability of HCC possibly through up-regulation of its potential effector PREX2.