No abstract

No abstract

No abstract

No abstract

No abstract

No abstract

Recently, studies on transcriptome-proteome relationships have revealed mRNA/protein expression discordance for certain genes and speculated that protein posttranslational modification (PTM) may be involved. However, there is currently no evidence to support this hypothesis. Wnt-induced secreted protein-1 (WISP1) is the downstream target gene of β-catenin and plays an important role in tumorigenesis and progression, but the expression and role of WISP1 in different tumor types are controversial. Here, we first confirmed that WISP1 protein expression was significantly down-regulated in hepatocellular carcinoma (HCC) tissue and could be an independent predictor of poor prognosis for patients with HCC. In vivo and in vitro evidence was provided that WISP1 can suppress HCC cell proliferation. Further studies have found that low WISP1 protein expression was related to expression of human leukocyte antigen F locus adjacent transcript 10 (FAT10), a specific ubiquitin-like protein with both degradation and stabilization functions, which plays an important role in PTM. FAT10 overexpression facilitated WISP1 degradation by FAT10ylation to decrease WISP1 protein expression, thus promoting HCC proliferation. Interestingly, we found and demonstrated that FAT10 overexpression could result in WISP1 protein/mRNA expression discordance, with protein expression decreasing while mRNA expression increased. The underlying mechanism is that FAT10 exerts substrate stabilization and degradation functions simultaneously, while FAT10 overexpression promotes WISP1 mRNA expression by stabilizing β-catenin and directly degrades WISP1 protein. Conclusion: Our study demonstrated that overexpression of FAT10 results in expression discordance between WISP1 protein and mRNA, thereby promoting HCC progression by down-regulating WISP1 protein expression.

Porous hollow-structural Co3O4 micropolyhedra were prepared by direct pyrolysis of zeolitic imidazolate framework (ZIF)-67 crystals in air. The Co3O4 primary nanoparticles and pore diameters increase with increasing calcination temperatures. Compared with the single Co3O4-350 catalyst, CO oxidation activity is greatly enhanced over the interface Ag/Co3O4-350 catalyst (T 100 = 120 °C and 8.8 × 10–2 molCO nm–2 s–1), which can be attributed to the improvement in surface-active oxygen and their mobility at the interface between Ag and Co3O4. The DRIFTS results proposed the CO oxidation reaction mechanism over the Ag/Co3O4 interface catalyst, and the formed Ag compound with surface oxygen species is more active for CO oxidation. The interface between Ag and Co3O4 facilitates both the oxygen activation and CO adsorption, hence lowering the reaction energy barrier and boosting the CO oxidation performance.