Heavy metal pollution such as water contamination by Pb, Hg, Cu, Cd and Cr ions is induced by rapid urbanization and industrialization and is a major threat to human health. One of the most efficient processes to clean contaminated water is adsorption. Adsorbents such as clay minerals and modified clays are efficient for the removal of metal ions from wastewater. This manuscript reviews current research in heavy metal adsorption by clay minerals such as halloysite, bentonite, montmorillonite, vermiculite and attapulgite, from 2013 to 2017, and highlights the main adsorption mechanisms. The structure, composition and synthesis of various clay minerals and modified clays are presented.

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Sox2 is a major transcription factor essential to the stemness characteristics and is associated with various types of cancers. In this study, we investigated the expressions and functional roles of Sox2 in hepatocellular carcinoma (HCC). Our data show that high level of Sox2 expression correlates with metastasis and low survival rate in HCC. HCC cells overexpressing Sox2 are characterized by active epithelial-mesenchymal transition and exhibit increased ability of transwell invasion, soft agar colonization, and sphere formation. We also found Sox2 expression was correlated with the transcription activity of SLUG promoter region. These results present novel mechanistic insight into an important role of Sox2 in HCC and suggest a potential application of Sox2 in HCC prognosis and treatment.

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Background-Aberrant activity of tyrosine-phosphorylated proteins is commonly associated with HCC metastasis. Cell signaling events driven by these proteins are implicated in numerous processes that alter cancer cell behavior. Exploring the activities and signaling pathways of these proteins in HCC metastasis may help in identifying new candidate molecules for HCC-targeted therapy.Methods-Hep3B (a nonmetastatic HCC cell line) and MHCC97H (a highly metastatic HCC cell line) were used in this study, and the tyrosine-phosphorylated proteins expressed in these cell lines were profiled by a phosphoproteomics technique based on LC-MS/MS. Protein-protein interaction and functional clustering analyses were performed to determine the activities of the identified proteins and the signaling pathways closely related to HCC metastasis.Results-In both cell lines, a total of 247 phosphotyrosine (pTyr) proteins containing 281 pTyr sites were identified without any stimulation. The involvement of almost 30% of these in liver or liver cancer has not been reported previously. Biological process clustering analysis indicated that pTyr proteins involved in cell motility, migration, protein autophosphorylation, cell-cell communication, and antiapoptosis functions were overexpressed during metastasis. Pathway clustering analysis revealed that signaling pathways such as those involved in EGFR signaling, cytokine- and chemokine-mediated signal transduction, and the PI3K and JAK-STAT cascades were significantly activated during HCC metastasis. Moreover, noncanonical regulation of the JNK cascade might also provide new targets for HCC metastasis. After comparing the pTyr proteins that were differentially expressed during HCC cell metastasis, we selected FER, a nonreceptor tyrosine kinase, and validated its role in terms of both expression and function. The data confirmed that FER might play a critical role in the invasion and metastasis of HCC.Conclusion-The identification of pTyr proteins and signaling pathways associated with HCC metastasis could provide useful information for selecting new molecular intervention targets. Moreover, FER might serve as a novel drug target in future HCC therapy.

Background and ObjectiveDue to recurrence and metastasis, the mortality of Hepatocellular carcinoma (HCC) is high. It is well known that the epithelial mesenchymal transition (EMT) and glycan of cell surface glycoproteins play pivotal roles in tumor metastasis. The goal of this study was to identify HCC metastasis related differential glycan pattern and their enzymatic basis using a HGF induced EMT model.MethodologyHGF was used to induce HCC EMT model. Lectin microarray was used to detect the expression of cell surface glycan and the difference was validated by lectin blot and fluorescence cell lectin-immunochemistry. The mRNA expression levels of glycotransferases were determined by qRT-PCR.ResultsAfter HGF treatment, the Huh7 cell lost epithelial characteristics and obtained mesenchymal markers. These changes demonstrated that HGF could induce a typical cell model of EMT. Lectin microarray analysis identified a decreased affinity in seven lectins ACL, BPL, JAC, MPL, PHA-E, SNA, and SBA to the glycan of cell surface glycoproteins. This implied that glycan containing T/Tn-antigen, NA2 and bisecting GlcNAc, Siaα2-6Gal/GalNAc, terminal α or βGalNAc structures were reduced. The binding ability of thirteen lectins, AAL, LCA, LTL, ConA, NML, NPL, DBA, HAL, PTL II, WFL, ECL, GSL II and PHA-L to glycan were elevated, and a definite indication that glycan containing terminal αFuc and ± Sia-Le, core fucose, α-man, gal-β(α) GalNAc, β1,6 GlcNAc branching and tetraantennary complex oligosaccharides structures were increased. These results were further validated by lectin blot and fluorescence cell lectin-immunochemistry. Furthermore, the mRNA expression level of Mgat3 decreased while that of Mgat5, FucT8 and β3GalT5 increased. Therefore, cell surface glycan alterations in the EMT process may coincide with the expression of glycosyltransferase.ConclusionsThe findings of this study systematically clarify the alterations of cell surface glycan in cancer EMT, and may provide novel insight for HCC metastasis.

Human haptoglobin is a serum glycoprotein secreted by the liver with four potential N-glycosylation sites on its β chain. Many studies have reported glycan changes of haptoglobin in diseases such as breast cancer and pancreatic cancer. The objective of our study is to analyze N-linked glycan alterations of serum haptoglobin β chain obtained from patients with the hepatitis B virus (HBV), liver cirrhosis (LC) and hepatocellular carcinoma (HCC). MALDI-QIT-TOF mass spectrometry revealed the intensity of m/z 1809.6, identified as a fucosylated glycan, was much higher in samples from patients with LC and HCC relative to the patients with HBV and healthy controls. Compared with LC patients, triantennary glycan was elevated and the biantennary structure was decreased in the haptoglobin β chain of HCC patients. Thus, alterations in the glycan structure of the haptoglobin β chain may constitute significant spectral signatures of cirrhosis and HCC disease.

Clusterin (CLU) is a stress-activated chaperone, which plays an important role in cancer development and progression through promoting cell survival. However, the exact mechanism of how CLU exerts its cell protective role under ER stress condition is still unclear. Therefore, in order to explore the molecular mechanisms by which CLU inhibited ER stress-induced apoptosis, HCC cell lines were treated with tunicamycin (TN), an ER stress inducer. We found that the expressions of both CLU and GRP78 were increased after TN treatment. Knockdown of CLU expression in SMMC7721 and HCCLM3 cells inhibited GRP78 expression after TN treatment and enhanced ER stress-induced apoptosis, whereas over-expression of CLU in HepG2 cells increased GRP78 expression after TN induction and abolished the effect of TN on cell apoptosis. Furthermore, knockdown of GRP78 expression in CLU-HepG2 cells abrogated the protective role of CLU under ER stress condition. Co-immunoprecipitation (co-IP) and confocal microscopy experiments confirmed the direct interaction between CLU and GRP78 under ER stress condition. The effect of CLU knockdown on GRP78 expression and cell apoptosis in HCC tumors were further determined in orthotopic xenograft tumor model. Knockdown of CLU expression in HCCLM3 cells inhibited GRP78 expression in tumor tissues, accompanied with increased number of apoptotic cancer cells. Moreover, the correlation between CLU and GRP78 expression was further determined in clinical HCC specimens. Taken together, these findings reveal that CLU protects HCC cells from ER stress induced apoptosis at least partially through interacting with GRP78.