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The Miaoya syenite and carbonatite complex is located in the southern margin of the South Qinling belt, central China. LA‐ICP‐MS zircon U–Pb dating reveals that the syenite and carbonatite have crystallization ages of 445.2 ± 2.6 Ma (MSWD = 0.66) and 434.3 ± 3.2 Ma (MSWD = 1.08), respectively. Both syenite and carbonatite display low ISr values (0.7004 to 0.7053) and depleted εNd(t) values of +1.1 to +5.5, with one‐stage Nd model ages of 0.65 to 0.94 Ga. Their zircon εHf(t) values are also similarly positive (+3.1 to +8.9), and one‐stage Hf model ages range from 0.71 to 0.92 Ga. Whole‐rock geochemistry suggests that the syenite belongs to the shoshonitic series and both syenite and carbonatite show identical REE and trace element patterns. The coeval intrusive ages, similar geochemical and Sr–Nd–Hf isotopic compositions suggest that the Miaoya carbonatite and associated syenite are genetically related to each other. We consider that the carbonatite could be a final product by protracted fractionation of a CO2‐rich alkaline melt. The depleted εNd(t) and zircon εHf(t) isotopes also indicate that the associated syenite and carbonatite could be originated from a mantle‐derived magma. The sources are likely composed of dominated HIMU mantle and minor EMI mantle. We propose that the Silurian Miaoya Complex was formed in the extensional rifting setting, associated with the mantle upwelling. Copyright © 2016 John Wiley & Sons, Ltd.

Objectives The purpose of this study was to investigate the association of PNPLA3 single nucleotide polymorphisms (SNPs) (rs738409 C > G, rs3747207 G > A, rs4823173 G > A, and rs2896019 T > G) with hepatocellular carcinoma (HCC) susceptibility. Methods This case–control study included 484 HCC patients and 487 controls. Logistic regression analysis was performed to study the associations of PNPLA3 gene polymorphisms with HCC susceptibility, and odds ratios with their corresponding 95% confidence intervals were calculated to evaluate these correlations. Results In the overall analysis, we found that the G allele (OR = 1.25, 95% CI = 1.04–1.50, p = 0.018, false discovery rate (FDR)-p = 0.035) and GG genotype (OR = 1.59, 95% CI = 1.06–2.39, p = 0.024, FDR-p = 0.048) of rs2896019 were significantly associated with increased HCC susceptibility. In stratified analysis, we found that all four SNPs were related to increased HCC susceptibility in subjects aged > 55 years. In haplotype analysis, the GAAG haplotype was significantly associated with increased HCC susceptibility (OR = 1.25, 95% CI = 1.03–1.53, p = 0.023, FDR-p = 0.046). Besides, we noticed that rs738409 was significantly correlated with alpha-fetoprotein (AFP) (p = 0.007), and HCC patients with the GG genotype had a higher level of AFP. Conclusions Our study suggested that PNPLA3-rs2896019 was significantly associated with an increased susceptibility to HCC.

Background Primary liver cancer (PLC) is the second leading cause of cancer-related death worldwide. It has been reported that PLC can be originated from malignant transformed adult hepatic progenitor cells. Mammalian large tumor suppressor kinase 1 (LATS1) is one of the core components of the Hippo pathway and it has been implicated in regulating invasion and metastasis of different cancer cell. However, the underlying connections between hepatic progenitor cells and LATS1 in the pathogenesis of PLC are still elusive. Methods LATS1 gene knockout (LATS1-KO) hepatic oval cells (HOCs) were constructed by the CRISPR/Cas9 system. Cell viability was evaluated by the CCK-8 assay. Cell migration was measured by scrape assay. Cell invasion was examined by Transwell assay. Cell apoptosis was evaluated by flow cytometry. The expression of LATS1 and Yes-associated protein (YAP) in HOCs was determined by Q-PCR and Western blot analysis. Results Here, we found that knockout of LATS1 significantly induced the migration and invasion of WB-F344 cells. Knockdown of YAP suppressed the neoplastic phenotype of LATS1-KO WB-F344 cells. Furthermore, overexpression of YAP promoted the migration and invasion of LATS1-KO WB-F344 cells. Conclusions In summary, the current study demonstrated that LATS1 is required for inhibiting the neoplastic phenotype of normal hepatic progenitor cell via downregulating YAP.