Timing and Spectral Analysis of the Black Hole X-Ray Binary MAXI J1803-298 with Insight-HXMT Data

We present a comprehensive analysis of the 2021 outburst of MAXI J1803–298 utilizing observations of the Insight-Hard X-ray Modulation Telescope(Insight-HXMT)spanning from the low hard state to the high soft state.Within the Insight-HXMT data set,compared to the previous work,we identify a more prolonged presence of typeC quasi-periodic oscillations(QPOs)with centroid frequencies ranging from~0.16 to 6.3 Hz,which present correlations with the hardness ratio and the photon index of the Comptonized component.For QPO frequencies less than~2 Hz,the QPO phase lags are hard(photons of 10–19 keV arrive later than those of 1–4 keV),while at higher frequencies,the lags become soft at and above~4 Hz.Furthermore,the spectra in all Insight-HXMT observations consist of a multi-color blackbody component and a Comptonized component,as commonly observed in classical black hole X-ray binaries.We analyze state transitions and the evolution of accretion geometry in this work.The fitted inner disk radius increases abnormally during the low hard state,hypothesized to result from the corona condensing onto the inner disk.Additionally,two significant drops in flux are observed during the soft intermediate state,maybe implying changes in the corona/jet and the disk,respectively.

Temporal and Spectral Characteristics of Persistent Emission and Special Bursts of Magnetar SGR J1935+2154 Based on Insight-HXMT

In October 2022,the magnetar SGR J1935+2154 entered the active outburst state.During the episode,the InsightHXMT satellite carried out a long observation that lasted for 20 days.More than 300 bursts were detected,and a certain amount of persistent radiation signals were also accumulated.This paper mainly introduces the results of persistent radiation profile folding and period search based on Insight-HXMT data.At the same time,the burst phase distribution characteristics,spectral lag results of burst,the spectral characteristics of zero-lag bursts and the time-resolved spectral evolution characteristics of high-flux bursts are reported.We found that there is no significant delay feature during different energy bands for the bursts of SGR J1935+2154.The observed zero-lag burst does not have a unique spectrum.The time-resolved spectrum of the individual burst has consistent spectral types and spectral parameters at different time periods of the burst.We also find that the burst number phase distribution and the burst photon phase distribution have the same tendency to concentrate in specific regions of the persistent emission profile.

Burst Phase Distribution of SGR J1935+2154 Based on Insight-HXMT

On 2020 April 27,the soft gamma-ray repeater SGR J1935+2154 entered its intense outburst episode again.Insight-HXMT carried out about one month observation of the source.A total number of 75 bursts were detected during this activity episode by Insight-HXMT,and persistent emission data were also accumulated.We report on the spin period search result and the phase distribution of burst start times and burst photon arrival times of the Insight-HXMT high energy detectors and Fermi/Gamma-ray Burst Monitor(GBM).We find that the distribution of burst start times is uniform within its spin phase for both Insight-HXMT and Fermi/GBM observations,whereas the phase distribution of burst photons is related to the type of a burst’s energy spectrum.The bursts with the same spectrum have different distribution characteristics in the initial and decay episodes for the activity of magnetar SGR J1935+2154.

Knockdown of Decoy Receptor 3 Impairs Growth and Invasiveness of Hepatocellular Carcinoma Cell Line of HepG2

Background：Decoy receptor 3 （DcR3） binds to Fas ligand （FasL） and inhibits FasL-induced apoptosis.The receptor is overexpressed in hepatocellular carcinoma （HCC）,and it is associated with the growth and metastatic spread of tumors.DcR3 holds promises as a new target for the treatment of HCC,but little is known regarding the molecular mechanisms underlying the oncogenic properties of DcR3.The present work,therefore,examined the role of DcR3 in regulating the growth and invasive property of liver cancer cell HepG2.Methods：HepG2 cells were stably transfected with lentivirus-based short hairpin RNA vector targeting DcR3.After the knockdown of DcR3 was confirmed,cell proliferation,clone formation,ability of migrating across transwell membrane,and wound healing were assessed in vitro.Matrix metalloproteinase-9 （MMP 9） and vascular epithelial growth factor （VEGF）-C and D expressions of the DcR3 knockdown were also studied.Comparisons between multiple groups were done using one-way analysis of variance （ANOVA）,while pairwise comparisons were performed using Student＇s t test.P 〈 0.05 was regarded statistically significant.Results：DcR3 was overexpressed in HepG2 compared to other HCC cell lines and normal hepatocyte Lo-2.Stable knockdown of DcR3 slowed down the growth of HepG2 （P 〈 0.05） and reduced the number of clones formed by 50% compared to those without DcR3 knockdown （P 〈 0.05）.The knockdown also reduced the migration of HepG2 across transwell matrix membrane by five folds compared to the control （P 〈 0.05） and suppressed the closure of scratch wound （P 〈 0.05）.In addition,the messenger RNA levels of MMP 9,VEGF-C,and VEGF-D were significantly suppressed by DcR3 knockdown by 90% when compared with the mock control （P 〈 0.05）.Conclusions：Loss of DcR3 impaired the growth and invasive property of HCC cell line of HepG2.Targeting DcR3 may be a potential therapeutic approach for the treatment of HCC.

Anti-apoptosis Effect of Decoy Receptor 3 in Cholangiocarcinoma Cell Line TFK-1

Background： Decoy receptor 3 （DcR3） is a protein with anti-apoptotic effect that belongs to the tumor necrosis factor receptor superfamily. DcR3 is highly expressed in a variety of malignant tumors including cholangiocarcinoma and its expression was found to be related to the clinical stage, the invasion, and tile metastasis of the tumor. This in vitro study aimed to investigate the effect ofdownregulated expression of DcR3 on cell viability, cell apoptosis, and cell cycle in cholangiocarcinoma cell line TFK-1. Methods： Three different cell lines were cultured： human cholangiocarcinoma TFK-I, human biliary epithelial carcinoma HuCCT-1, and human cholangiocarcinoma RBE. The cholangiocarcinoma cell line with the highest expression of DcR3 was selected for further investigation. The expression of DcR3 was silenced/knocked down by transfection with DcR3-siRNA in the selected cell line. Various biological phenotype parameters such as cell viability, apoptosis, and cell cycle were observed. Results： The mRNA and protein levels of DcR3 were measured in the three cell lines, and TFK-1 was selected. After the treatment with DcR3-siRNA for 48 h, DcR3 mRNA and protein expression in the treatment group were 38.45% （P 〈 0.01 ） and 48.03% （P 〈 0.05） of that of＇the control, respectively. It was found that the cell viability decreased to 61.87% of the control group （P 〈 0.01 ） after the downregulation of DcR3 in cholangiocarcinoma cell line TFK- 1 by transfection with DcR3-siRNA, while tile percentage ofapoptotic cells was 2.98 times as compared with the control group （P 〈 0.05）. Compared with the control group the ratio of G0/G1 increased, and the ratio of G2/M dccreased in the treatment group. However, the differences were not statistically significant. Conclusions： The effect of DcR3 on the growth and apoptosis ofcholangiocarcinoma has been demonstrated. DcR3 is not only a predictive marker for malignant tumor but it is also likely to be a potential target for cancer gene therapy. Further studies should focus on exploring the binding ligand of DcR3, the signaling pathway involved, and the molecular mechanism for the regulation of DcR3 expression in cholangiocarcinoma.

XB130 Knockdown Inhibits the Proliferation, Invasiveness, and Metastasis of Hepatocellular Carcinoma Cells and Sensitizes them to TRAIL-Induced Apoptosis

Background：XB 130 is a recently discovered adaptor protein that is highly expressed in many malignant tumors,but few studies have investigated its role in hepatocellular carcinoma （HCC）.Therefore,this study explored the relationship between this protein and liver cancer and investigated its molecular mechanism of action.Methods：The expression of XB 130 between HCC tissues and adjacent nontumor tissues was compared by real-time polymerase chain reaction,immunochemistry,and Western blotting.XB130 silencing was performed using small hairpin RNA.The effect of silencing XB130 was examined using Cell Counting Kit-8,colony assay,wound healing assay,and cell cycle analysis.Results：We found that XB 130 was highly expressed in HCC tissues （cancer tissues vs.adjacent tissues：0.23 ± 0.02 vs.0.17 ± 0.02,P 〈 0.05） and liver cancer cell lines,particularly MHCC97H and HepG2 （MHCC97H and HepG2 vs.normal liver cell line LO-2：2.35 ± 0.26 and 2.04 ± 0.04 vs.1.00 ± 0.04,respectively,all P 〈 0.05）.The Cell Counting Kit-8 assay,colony formation assay,and xenograft model in nude mice showed that silencing XB130 inhibited cell proliferative ability both in vivo and in vitro,with flow cytometry demonstrating that the cells were arrested in the G0/G1 phase in HepG2 （HepG2 XB130-silenced group [shA] vs.HepG2 scramble group [NA]：74.32 ± 5.86% vs.60.21 ± 3.07%,P 〈 0.05） and that the number of G2/M phase cells was decreased （HepG2 shA vs.HepG2 NA：8.06 ± 2.41% vs.18.36 ± 4.42%,P 〈 0.05）.Furthermore,the cell invasion and migration abilities were impaired,and the levels of the epithelial-mesenchymal transition-related indicators vimentin and N-cadherin were decreased,although the level of E-cadherin was increased after silencingXB130.Western blotting showed that the levels of phosphorylated phosphoinositide 3-kinase （PI3K） and phospho-protein kinase B （p-Akt） also increased,although the level of phosphorylated phosphatase and tensin homolog increased,indicating that XB 130 activated the PI3K/ Akt pathway.Furthermore,we found that a reduction in XB130 increased liver cancer cell sensitivity to tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis.Conclusions：Our findings suggest that XB130 might be used as a predictor of liver cancer as well as one of the targets for its treatment.