Fate of microplastics in deep-sea sediments and its influencing factors: Evidence from the Eastern Indian Ocean.

Although microplastics (MPs) are known to be found in global oceans, their influencing factors and abundance in the deep sea remain largely unknown. Twenty-six surface sediment samples were collected in the deep basin of the Eastern Indian Ocean (EIO). This study showed that MPs abundance ranged from 30.30 particles/kg to 701.7 particles/kg, with an average of 170.5 ± 140.2 particles/kg. The MPs found in the sediment of the EIO mainly contain fragments and fibers, which account for 47.5% and 45.6%. The MPs were measured in a size range of 44-5000 µm, and the most frequently detected MPs in size of 200-500 µm. MPs were in various compositions, but most of them were found in rayon (62.2%) and polyester (25.7%). The spatial distribution of MPs in the sediments shows a decreasing trend from nearshore to the open sea. In the Bay of Bengal (BOB) and the coast of Sri Lanka (COSL), the abundance of MPs was relatively high, indicating that the spatial distribution of MPs is affected by land source input, river input, and anthropogenic activities. Principal component analysis indicated daily commodities and packaging applications/fishing accounted for 36.9% and 12.9% of the MPs occurrence in the EIO, respectively. Average MPs diversity indices for the BOB (0.87 ± 0.38), the COSL (0.64 ± 0.56), and the Eastern Indian Ocean Basin (EIOB) (0.60 ± 0.24) revealed the BOB had the most complicated MPs sources. In addition, we found that the abundance of MPs has no significant effect on organic carbon and sediment grain size. This study is the first report of MPs detection in the deep-sea sediment in the EIO and can provide a baseline of MPs pollution in this area.

Assessment and sources identification of microplastics, PAHs and OCPs in the Luoyuan Bay, China: Based on multi-statistical analysis.

Luoyuan Bay is a mariculture influenced water body located in southeastern China. Multi-statistical techniques were applied to 21 sampling locations in the bay to identify the sources of microplastics and other pollutants in the sediment. In microplastics detection, fragment was the most abundant shape (~36%), and rayon was the dominant polymer (~59%). The size of more than 48% of total microplastics observed was less than 200 µm. The study showed that the upper part of Luoyuan Bay was dominated by microplastic pollution, while the lower part of the bay was dominated by persistent organic pollutants (PAHs, OCPs). Mariculture is one of the main sources of pollution in Luoyuan Bay. Apart from mariculture, there were additional sources such as industry, land reclamation, port, and so on; industry and land reclamation were the leading sources of microplastics, while port, industry, and mariculture were the primary sources of PAHs and OCPs.

CD147 confers temozolomide resistance of glioma cells via the regulation of ß-TrCP/Nrf2 pathway.

Background: Drug resistance is one of the biggest challenges in cancer therapy. temozolomide (TMZ) represents the most important chemotherapeutic option for glioma treatment. However, the therapeutic efficacy of TMZ remains very limited due to its frequent resistance in glioma, and the underlying mechanisms were not fully addressed. Herein, we demonstrate that the elevated expression of CD147 contributes to TMZ resistance in glioma cells, potentially through the post-translational regulation of Nrf2 expression. Methods: Cell-based assays of CD147 triggered drug resistance were performed through Edu-incorporation assay, CCK8 assay, TUNEL staining assay and flow cytometric assay. Luciferase reporter assay, protein stability related assays, co-immunoprecipitation assay were used to determine CD147 induction of Nrf2 expression through ß-TrCP dependent ubiquitin system. Finally, the effect of the CD147/Nrf2 signaling on glioma progression and TMZ resistance were evaluated by functional experiments and clinical samples. Results: Based on the analysis of clinical glioma tissues, CD147 is highly expressed in glioma tissues and positively associated with tumor malignancy. Suppression of CD147 expression increased the inhibitory effect of TMZ on cell survival in both U251 and T98G cells, whereas the gain of CD147 function blocked TMZ-induced ROS production and cell death. Mechanistic study indicates that CD147 inhibited GSK3ß/ß-TrCP-dependent Nrf2 degradation by promoting Akt activation, and subsequently increased Nrf2-mediated anti-oxidant gene expressions. Supporting the biological significance, the reciprocal relationship between CD147 and Nrf2 was observed in glioma tissues, and associated with patient outcome. Conclusions: Our data provide the first evidence that glioma resistance to TMZ is potentially due to the activation of CD147/Nrf2 axis. CD147 promotes Nrf2 stability through the suppression of GSK3ß/ß-TrCP dependent Nrf2 protein degradation, which results in the ablation of TMZ induced ROS production. As such, we point out that targeting CD147/Nrf2 axis may provide a new strategy for the treatment of TMZ resistant gliomas.

SUMOylation of HSP27 by small ubiquitin-like modifier 2/3 promotes proliferation and invasion of hepatocellular carcinoma cells.

Primary hepatocellular carcinoma (PHC) is a major health problem worldwide and is one of the 10 most commonly diagnosed cancers in China. Heat shock protein 27 (HSP27) were found to be overexpressed in a wide range of malignancies including PHC, however, post-translational modification of HSP27 still needs exploration in PHC. Recently, SUMOylation, an important post-translational modification associating with the development of many kinds of cancers has been intensively studied. In the current study, mRNA and protein level of HSP27 in archived tumor samples representing various pathological characteristics of PHC were examined, and modification of HSP27 by SUMO2/3 was investigated. HSP27 were expressed abundantly in patients' tumor tissues, and found to be associated with pathological progression. Besides, HSP27 was also elevated significantly in liver cancer cell lines Huh7 and HepG2 compared with human hepatocyte cells L02. Furthermore, knockdown of HSP27 was found to be associated with the decreased proliferation and invasion ability in Huh7 and HepG2 cells. Immunofluorescence assay showed that HSP27 and SUMO2/3 were co-localized in the subcellular, and co-immunoprecipitation verified the interaction between HSP27 and SUMO2/3. Overexpression of SUMO2/3 upregulated the HSP27 protein level and promotes Huh7 and HepG2 cell proliferation and invasion, and vice versa when the SUMO2/3 was knockdown. Taken together, increased protein level of HSP27 through SUMO2/3-mediated SUMOylation plays crucial roles in the progression of PHC, and this finding may shed light on developing potential therapeutic targets for PHC.