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Published in Valerio Voliani, Nanomaterials and Neoplasms, 2021
Eun-Kyung Lim, Taekhoon Kim, Soonmyung Paik, Seungjoo Haam, Yong-Min Huh, Kwangyeol Lee
Gene therapy is the use of genes as medicine that involves the transfer of a therapeutic or working gene (DNA and RNA) copy into specific cells of a patient in order to repair gene defects due to mutations [403–409, 413, 420–426]. This technique has been studied in clinical settings for a variety of cancer types and other disease involving gene defects. Cancer cells possess upregulated or inappropriately expressed genes, which leads to uncontrolled cell growth. Identification of target genes could lead to development of tailored anticancer agents with which the toxic side effect of cancer chemotherapies could be overcome. For example, RNAi-based gene therapies, i.e., sequence-specific post-transcriptional silencing of gene expression mediated by small double-stranded (dsRNA), have the potential to treat a variety of human genomic disorder, especially in combination with conventional therapies such as chemotherapy [419, 424]. Whereas knockdown of a target mRNA is not feasible with sense and antisense RNAs, dsRNA can lead to an effective and a specific mRNA knockdown. After dsRNA is introduced into cells it is cleaved by the enzyme dicer, a member of the RNaseIII family of dsRNA-specific ribonucleases [407, 409, 421, 424]. This enzymatic cleavage degrades the RNA to 19–23 bp duplexes, each with a 2-bp 3′ overhang [703, 408, 422].
A review of quorum sensing regulating heavy metal resistance in anammox process: Relations, mechanisms and prospects
Published in Critical Reviews in Environmental Science and Technology, 2023
Caiyan Qu, Fan Feng, Jia Tang, Xi Tang, Di Wu, Ruiyang Xiao, Xiaobo Min, Chong-Jian Tang
QS enhances the synthesis of electron shuttles to mediate the electron transfer during the redox transformation of heavy metals. The cytochrome c protein containing heme c approximately accounts for 20% of the cellular proteins in anammox cells, which participates in electron transfer of anammox respiratory chain (Wang & Zheng, 2017; Feng et al., 2022). AHL addition significantly upregulated the expression of genes encoding cytochrome P450 and cytochrome c precursor, resulting in an increased production of these cytochrome. The cytochrome facilitated the electron transfer from intracellular ubiquinone to the cytoplasmic space (Whiteley et al., 1999). Additionally, AHL increased the NAD level of anammox consortia in the metabolite analysis, suggesting that AHL-mediated QS could increase the amount of electron shuttles (Tang et al., 2018b). Subsequently, cytochrome c and NADH (the reduction state of NAD) were reported to catalyze V(V) and Cr(VI) reduction to V(IV) and Cr(III), respectively (Shi et al., 2020).
Association of occupational exposure to pesticides with overweight and abdominal obesity in family farmers in southern Brazil
Published in International Journal of Environmental Health Research, 2022
Roberta Andressa Line Araújo, Cleber Cremonese, Ramison Santos, Camila Piccoli, Gabriela Carvalho, Carmen Freire, Raquel Canuto
Regarding insecticides and the outcomes of interest, only animal models and in vivo studies were found in the literature. An animal model study exposed mice to bifenthrin, a synthetic pyrethroid, for 6 weeks, resulting in increased body weight and fat mass. Hormone-sensitive protein lipase and adipose triglyceride lipase were downregulated, whereas lipoprotein lipase was upregulated after treatment. Similar effects were seen in 3T3-L1 cells treated with bifenthrin, thus validating the in vivo results (Wei et al. 2019). Similar results were also seen in cell models treated with cis-bifenthrin in a study conducted by Xiang et al. (2018) (Xiang et al. 2018). Shen et al. (2017) demonstrated that deltamethrin, a pyrethroid, increased the fat accumulation in 3T3-L1 adipocytes and Caenorhabditis elegans via aak-2 (an ortholog of AMPKα)-mediated mechanisms in an animal model (Shen et al. 2017). The results of these studies suggest that long-term exposure to pyrethroid insecticides disrupts the processes of fatty acid uptake and lipolysis, thus inducing fat deposition, which could cause obesity in humans as well.
In vitro and in vivo estrogenic activity of triclosan
Published in Journal of Toxicology and Environmental Health, Part A, 2021
Kyung Sik Yoon, Seung Jun Kwack
To determine whether cellular processes affected by TCS and E2 are also shared enrichment analysis was conducted for gene ontology biological processes (GOBPs) for the genes upregulated and downregulated by TCS and E2 (Huang, Sherman, and Lempicki 2009). Of the GOBPs, many processes related to apoptosis (cell death and regulation of growth), metabolism (sterol/steroid and hexose metabolic processes), and RNA/protein homeostasis (RNA processing and protein folding/localization) were commonly upregulated by TCS and E2 (Figure 4). In contrast, processes related to oxidation reduction and extracellular matrix organization were commonly downregulated by TCS and E2. Importantly, the process related to estrogen (response to estrogen stimulus) was commonly altered by E2 and TCS (Figure 4). The GOBPs altered in the TCS-treated group and associated with the uterine-weight-increasing effects of estrogen are presented in Table 3.