Introduction Enhancer of zeste homolog 2 (EZH2) is implicated in hepatocellular carcinoma (HCC), but whether transforming growth factor-β (TGF-β)-metastasis associated 1 (MTA1)-SMAD7-SMAD3-SRY-Box Transcription Factor 4 (SOX4)-EZH2 signaling axis, in which EZH2 participates, is also involved in HCC remained unknown. Methods Data on EZH2 expression in liver hepatocellular carcinoma (LIHC) and its relation with prognosis of HCC patients were predicted and analyzed using online databases. Following transfection with or without TGF-β1, HCC cell viability, migration and invasion were determined with MTT, Scratch and Transwell assays. Relative expressions of epithelial-to-mesenchymal transition (EMT)-related factors (N-Cadherin, Vimentin, and E-Cadherin) and TGF-β-MTA1-SMAD7-SMAD3-SOX4-EZH2 signaling axis factors (TGF-β, MTA1, SMAD7, phosphorylated-SMAD3, SOX4 and EZH2) were calculated via reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and Western blot. Results EZH2 was upregulated in HCC, which was related to poor prognosis. Silencing EZH2 suppressed EZH2 expression and HCC cell viability, migration, and invasion, and increased E-Cadherin expression yet decreased N-Cadherin and Vimentin expression, whereas EZH2 overexpression did conversely. Also, silencing EZH2 reversed the effects of TGF-β1 on promoting viability, migration, and invasion, as well as N-Cadherin and Vimentin expressions, yet suppressing E-Cadherin expression in HCC cells. In addition, TGF-β1 promoted TGF-β, MTA1, SOX4 and EZH2 expressions and p-SMAD3/SMAD3 ratio yet suppressed SMAD7, whereas silencing EZH2 solely reversed the effects of TGF-β1 on EZH2 expression in HCC cells. Conclusion The present study provides a theoretical basis for TGF-β-MTA1-SMAD7-SMAD3-SOX4-EZH2 signaling cascade in viability, migration, invasion, and EMT of HCC cells. Inhibiting these signals may represent a therapeutic pathway for the treatment of metastatic HCC.

SBF2-AS1 is an oncogenic long non-coding RNA (lncRNA). However, its role and mechanism in hepatocellular carcinoma (HCC) is still not completely clear. The HepG2, Hep3B, Bel-7402 and HL-7702 cell lines were used in our experiments. The CCK-8 kit and EdU staining were applied to detect cell viability and multiplication. The wound healing and Boyden chamber cell migration assays were employed to test the migration ability of cells. The levels of TGF-β1 mRNA, lncRNA SBF2-AS1, and miR-361-5p were assessed by real-time PCR. TGF-β1 protein levels were evaluated by western blotting. The direct interaction between miR-361-5p and TGF-β1 was determined by luciferase reporter assays. A xenograft mouse model (XMM) was established to comprehensively study the effect and mechanisms of lncRNA SBF2-AS1. lncRNA SBF2-AS1 concentration in HCC cells exceeded that in a normal hepatocyte cell line. The downregulation of lncRNA SBF2-AS1 upregulated miR-361-5p levels in HCC cells. And, miR-361-5p negatively regulate TGF-β1 expression in HCC cells. The suppression of miR-361-5p attenuated the influence of lncRNA SBF2-AS1 downregulation on the viability, proliferation, and migration capability of HCC cells. Further, the downregulation of lncRNA SBF2-AS1 inhibited neoplasm growth in an XMM of HCC. Simultaneously, miR-361-5p was upregulated and TGF-β1 was downregulated after lncRNA SBF2-AS1 knocked down. In conclusion, downregulation of lncRNA SBF2-AS1 inhibits HCC proliferation and migration through the regulation of the miR-361-5p/TGF-β1 signaling pathway.

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The syndrome of ROU is generally manifested as obvious pain, redness, and swelling of local ulceration area, accompanied by flushed face, red eyes, sore throat, and swollen gums. Traditional Chinese medicine (TCM) doctors believe that “yin deficiency” is one causative factor of ROU. Zhibaidihuang decoction (ZBDHD) is a prescriptively developed receipt, where Anemarrhena asphodeloides and Phellodendri amurensis Cortex are added in the original Liuweidihuang decoction. It is generally used for “yin deficiency” treatment. It can effectively reduce the recurrence of oral ulcers and release the severity of the disease. However, the mechanism of this activity remains to be elucidated. In this study, we found that ZBDHD has a certain therapeutic effect on the pathological changes of oral mucosa. Furthermore, the results of serum metabolomics showed ZBDHD influenced the synthesis and metabolism of certain fatty acids. The results of western blot, immunochemical, and immunofluorescence staining indicate that ZBDHD could increase the expression of Sirt1 and Foxp3 and suppress the expression and acetylation of NF-κB in oral mucosa cells. By screening active ingredients in ZBDHD, we found berberine, as well as other compounds, presenting high fitness of the Sirt1 reactive centre. Therefore, it is possible that ZBDHD can regulate the Sirt1-NF-κB pathway to improve fatty acids metabolism in the body, thereby achieving the effect of treating ROU.

As a new type of non-volatile memory, quantum dots resistive random access memory (RRAM) has attracted much attention for its simplicity of preparation, fast responding time, high storage density, and smaller device size. CuInS₂ quantum dots (CuInS₂ QDs) are a kind of excellent resistive functional material with abundant electron capture sites, high optical absorption coefficient, and high carrier mobility. In this paper, CuInS₂ QDs/PNZT films were prepared by spin-coating CuInS₂ QDs on PNZT films. The results show that the resistive properties of CuInS₂ QDs RRAMs can be effectively improved by introducing PNZT films and can be controlled by altering the polarization direction. The CuInS₂ QDs/PNZT film in the negative polarization state promotes the interfacial electrons flowing to the PNZT film, which will reduce the height of the interfacial barrier and the thickness of the interfacial depletion region. And it will reduce the resistance of the composite film at the LRS. Compared to the switching voltage and resistive switching ratio of the pure CuInS₂ QDs film (10³), the switching voltage of the device is reduced to -4.1/3.4 V and the resistive switching ratio is increased to 10⁶. Furthermore, it maintains good stability in the 10³ cycle durability test. In contrast, the CuInS₂ QDs/PNZT film interface has a larger barrier height and depletion-layer thickness when the PNZT is in the positive polarization state, which increases the resistance of the composite film in the LRS state. As a result, the switching voltage of the device increases to -6.4/5.7 V with a resistive switching ratio of 104. The resistive properties of the CuInS₂ QDs/PNZT film can be tuned by changing the polarization direction, as the polarization direction of the PNZT changes the interfacial energy band structure and affects the conduction mechanism. This work reveals the feasibility of using ferroelectric thin films to improve the resistive properties of quantum dots RRAMs and providing further opportunities for the development of RRAMs.

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Background This study aimed to identify the biological functions, expression modes, and possible mechanisms underlying the relationship between metastatic human hepatocellular carcinoma (HCC) and MicroRNA-188-5p (miR-188) dysregulation using cell lines. Methods A decrease in miR-188 was detected in low and high metastatic HCC cells compared to that in normal hepatic cells and non-invasive cell lines. Gain- and loss-of-function experiments were performed in vitro to investigate the role of miR-188 in cancer cell (Hep3B, HepG2, HLF, and LM3) proliferation and migration. Results miR-188 mimic transfection inhibited the proliferation of metastatic HLF and LM3 cells but not non-invasive HepG2 and Hep3B cells; nonetheless, miR-188 suppression promoted the growth of HLF and LM3 cells. miR-188 upregulation inhibited the migratory rate and invasive capacity of HLF and LM3, rather than HepG2 and Hep3B cells, whereas transfection of a miR-188 inhibitor in HLF and LM3 cells had the opposite effects. Dual-luciferase reporter assays and bioinformatics prediction confirmed that miR-188 could directly target forkhead box N2 (FOXN2) in HLF and LM3 cells. Transfection of miR-188 mimics reduced FOXN2 levels, whereas miR-188 inhibition resulted in the opposite result, in HLF and LM3 cells. Overexpression of FOXN2 in HLF and LM3 cells abrogated miR-188 mimic-induced downregulation of proliferation, migration, and invasion. In addition, we found that miR-188 upregulation impaired tumor growth in vivo. Conclusions In summary, this study showed thatmiR-188 inhibits the proliferation and migration of metastatic HCC cells by targeting FOXN2.