Long non-coding RNA CDKN2B-AS1 promotes hepatocellular carcinoma progression via E2F transcription factor 1/G protein subunit alpha Z axis.

BACKGROUND: A series of long non-coding RNAs (lncRNAs) have been reported to play a crucial role in cancer biology. Some previous studies report that lncRNA CDKN2B-AS1 is involved in some human malignancies. However, its role in hepatocellular carcinoma (HCC) has not been fully deciphered. AIM: To decipher the role of CDKN2B-AS1 in the progression of HCC. METHODS: CDKN2B-AS1 expression in HCC was detected by quantitative real-time polymerase chain reaction. The malignant phenotypes of Li-7 and SNU-182 cells were detected by the CCK-8 method, EdU method, and flow cytometry, respectively. RNA immunoprecipitation was executed to confirm the interaction between CDKN2B-AS1 and E2F transcription factor 1 (E2F1). Luciferase reporter assay and chromatin immunoprecipitation were performed to verify the binding of E2F1 to the promoter of G protein subunit alpha Z (GNAZ). E2F1 and GNAZ were detected by western blot in HCC cells. RESULTS: In HCC tissues, CDKN2B-AS1 was upregulated. Depletion of CDKN2B-AS1 inhibited the proliferation of HCC cells, and the depletion of CDKN2B-AS1 also induced cell cycle arrest and apoptosis. CDKN2B-AS1 could interact with E2F1. Depletion of CDKN2B-AS1 inhibited the binding of E2F1 to the GNAZ promoter region. Overexpression of E2F1 reversed the biological effects of depletion of CDKN2B-AS1 on the malignant behaviors of HCC cells. CONCLUSION: CDKN2B-AS1 recruits E2F1 to facilitate GNAZ transcription to promote HCC progression.

[Effects of selective head cooling with mild hypothermia on serum levels of caspase-3 and IL-18 in neonates with hypoxic-ischemic encephalopathy].

OBJECTIVE: The study examined the changes of serum caspase-3 and IL-8 levels following selective head cooling with mild hypothermia (SHC) treatment in neonates with hypoxic-ischemic encephalopathy (HIE) in order to explore the mechanism of neuroprotection of SHC against HIE. METHODS: Thirty-three neonates with moderate or severe HIE were randomly assigned to two groups: SHC treatment (n=16) and conventional treatment (n=17). Serum levels of caspase-3 and IL-18 were measured using ELISA before treatment and 24 hrs, 48 hrs, 72 hrs and 5 days after treatment. RESULTS: Serum caspase-3 levels in the SHC group decreased 24 and 48 hrs after treatment (3.8±1.9 and 2.6±1.2 ng/mL, respectively) compared with 6.1±2.3 ng/mL at 24 hrs and 7.2±3.1 ng/mL at 48 hrs in the conventional treatment group (P<0.05). Serum IL-18 levels in the SHC group decreased 24 hrs, 48 hrs and 72 hrs after treatment (119±30, 76±33 and 71±40 ng/mL, respectively) compared with those in the conventional treatment group (138±28 ng/mL at 24 hrs, 156±60 ng/mL at 48 hrs and 182±54 ng/mL at 72 hrs; P<0.01). CONCLUSIONS: SHC treatment can inhibit the release of caspase-3 and the expression of IL-18 in neonates with moderate or severe HIE. This may contribute to the neuroprotection of SHC against HIE.

1H-MRSI of prostate cancer: the relationship between metabolite ratio and tumor proliferation.

PURPOSE: To investigate whether 1H-MRSI can be used to predict the proliferative activity of prostate cancer. MATERIALS AND METHODS: Thirty-eight patients with prostate cancer (PCa) and thirty-three patients with benign prostate hyperplasia (BPH) were included in this study. Patients were examined in supine position using a 1.5T superconducting magnetic scanner equipped with a pelvic phased-array multi-coil and CSI-3D-PROSTATE sequence. Commercial software was used to acquire and process MR spectroscopic imaging data. Mean (Cho+Cr)/Cit ratios of PCa, BPH, and peripheral zone (PZ) were calculated. Cellularity of PCa was recorded based on hematoxylin and eosin staining. PCNA was detected using immunohistochemical techniques. RESULTS: The mean (Cho+Cr)/Cit ratio of the peripheral zone (0.38+/-0.09) was lower than that of BPH (0.51+/-0.19) (P<0.05). The average value of (Cho+Cr)/Cit ratio of prostate cancer was 3.98+/-0.12. The (Cho+Cr)/Cit ratio of prostate cancer was higher than that of the peripheral zone and BPH (P<0.05). The cellularity and PCNA LI of prostate cancer were 12.90+/-4.07% and 72.1+/-19.01%, respectively. The (Cho+Cr)/Cit ratio of prostate cancer positively correlated with tumor cellularity (r=0.582, P=0.027) and PCNA LI (r=0.495, P=0.022). CONCLUSION: The (Cho+Cr)/Cit ratio of PCa can reveal the differences in proliferative activity between PCa and BPH. MRSIs are therefore able to predict the proliferative rate of variously differentiated prostate cancers.

Diffusion-weighted imaging of prostate cancer: correlation between apparent diffusion coefficient values and tumor proliferation.

PURPOSE: To investigate whether the apparent diffusion coefficient (ADC) values of prostate cancer (PCa) are able to reflect tumor proliferation. MATERIALS AND METHODS: The clinical and pathological information for 38 patients with PCa and 33 patients with benign prostate hyperplasia (BPH) were studied. Examination of the patients was performed using a 1.5 T superconducting magnetic scanner equipped with a pelvic phased-array multicoil. Diffusion-weighted images (DWIs) were acquired using an echo-planar imaging sequence. The ADC values of PCa, BPH, and peripheral zone (PZ) were calculated. The cellularity of PCa was recorded based on hematoxylin and eosin staining. The proliferating cell nuclear antigen (PCNA) was detected using an immunohistochemical technique. RESULTS: The ADC values of PCa, BPH, and PZ were 49.32 +/- 12.68 x 10(-5) mm(2)/s, 86.73 +/- 26.75 x 10(-5) mm(2)/s, and 126.25 +/- 27.21 x 10(-5) mm(2)/s, respectively. The ADC values of PCa were lower than those of BPH and PZ (P < 0.05). The cellularity and PCNA labeling index (LI) of PCa were higher than those of BPH (P < 0.05). The ADC values of PCa were negatively correlated with those of cellularity and PCNA LI (r = -0.646 and -0.446, respectively; P < 0.05). CONCLUSION: The ADC values of PCa can reveal the differences in proliferative activity between PCa and BPH. These values are therefore able to predict the proliferative rate of variously differentiated prostate cancers.