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Tea is consumed widely around the world owing to its refreshing taste and potential health benefits. However, drinking tea is considered a major route for dietary aluminum exposure in areas where tea consumption is relatively large. To assess the health risk associated with drinking tea, the contamination level of aluminum was determined in 81 tea samples. The transfer rate of aluminum during tea brewing was investigated. Then based on the site-specific exposure parameters such as consumption data and body weight for six different subpopulations in Fujian, the exposure risks were estimated using a probabilistic approach. Results demonstrate that the contents of aluminum in green tea, white tea, oolong tea, and black tea were significantly different according to the one-way ANOVA analysis (p < 0.05). The transfer rate of aluminum were 32.6%, 31.6%, 26.3%, and 14% for white tea, black tea, oolong tea, and green tea, respectively. With respect to the oral reference dose, the exposure of inhabitants in Fujian to aluminum through drinking tea is under control (even at the 99th percentile). [ABSTRACT FROM AUTHOR]

The objective of this study was to evaluate the residues of 42 pesticides subject to public concern in Tieguanyin tea produced in Fujian, China. The presence of 42 pesticide residues in 90 Tieguanyin tea samples were determined. A total of 17 pesticides were detected. At least one pesticide residue was detected in 65 samples (72.2%). The detected pesticides imidacloprid, tolfenpyrad, bifenthrin, acetamiprid were found in 55.6%, 33.3%, 18.9% and 16.7% of samples, respectively. Pesticide residues in Tieguanyin tea varied significantly over the seasons and across the production regions. Based on data obtained, the health risks associated with long-term exposure to those pesticides were assessed and risks of detected pesticides were ranked. The hazard quotients (HQs) among the detected pesticides range from 5 × 10−8 for fenpropathrin to 3 × 10−4 for imidacloprid. The results demonstrated that despite a high occurrence of pesticide residues in Tieguanyin tea, residue levels observed could not be considered as a serious public health problem. The risk ranking scheme showed dicofol and thiacloprid were considered to pose a medium-risk. The suggestions for 17 detected pesticides used in Tieguanyin tea plantation were made, including those already banned from use in China (dicofol and methomyl), recommended for diminished use (thiacloprid and chlorpyrifos), and permitted use with considering the pre-harvest interval (13 other pesticides). [ABSTRACT FROM AUTHOR]

Perchlorate is known as a thyroid disrupter. Its contamination in various tea samples was monitored, and 286 samples belonging to four types of tea leaves were analysed. The detection rate of perchlorate in tea was 99.3%. The mean concentration in different tea types decreased in order from green tea, oolong tea, white tea to black tea. A probabilistic approach was performed to evaluate the dietary exposure of perchlorate for six different subpopulations. The daily intakes (EDIs) for consumers over the age of 41 were higher than that of other subpopulations. The hazard quotient for six groups was lower than 1 even at the extreme percentile (P99). It indicates that the risk of dietary exposure to perchlorate from tea consumption for Fujian people is acceptable without considering other foodstuffs. However, the high occurrence of perchlorate in tea samples suggested that the actual source of this contaminant should be further investigated. [ABSTRACT FROM AUTHOR]

Sensitive, simple and quick methods for determination of dinotefuran, cyromazine, and the metabolites 1-methyl-3-(tetrahydro-3-furylmethyl) guanidine (DN), 1-methyl-3-(tetrahydro-3-furylmethyl) urea (UF), and melamine in Agrocybe aegerita were established and validated by ultra-performance liquid chromatography tandem mass spectrometry (UPLC-MS/MS). The dissipation and residues of these compounds in A. aegerita were investigated. The field results showed that dinotefuran and cyromazine dissipated rapidly with half-lives ranging from 24.9 h to 38.5 h. The terminal residues of total dinotefuran (the sum of dinotefuran and its metabolites), cyromazine, and melamine in fresh mushroom samples collected with sampling intervals of 3 d to 6 d ranged from 0.089 to 0.652 mg/kg, 0.593 to 2.054 mg/kg, and 0.002 to 0.005 mg/kg, respectively. During the drying processes of A. aegerita, the processing factors of dinotefuran, cyromazine, DN, UF, and melamine were 0.028, 0.012, 0.301, 0.002, and 0.001, respectively. Given that cyromazine and dinotefuran are not registered for use on A. aegerita , dietary risk was assessed. Based on a consumption survey, risk quotient (RQ) values significantly below 1 implied that the risk of A. aegerita consumption was acceptable, although the risk for children was relatively higher. The findings could provide valuable guidance for the appropriate use of these insecticides in A. aegerita cultivation and serve as a scientific reference for setting corresponding maximum residue limits (MRL) in China. [Display omitted] • Dinotefuran and cyromazine dissipated rapidly in Agrocybe aegerita cultivation. • The dietary risk was acceptable for consumption of Agrocybe aegerita. • Drying process clearly decreases residues of these compounds. • A guidance for the appropriate use of these insecticides was provided. [ABSTRACT FROM AUTHOR]

White tea has been of increasing public interest worldwide owing to its health benefits. Based on 2 years of surveillance, the long‐term and cumulative chronic exposure risks of pesticide residues through white tea drinking were assessed for different subpopulations in Fujian, China. Twenty‐five different pesticides were found, and 74.8% of samples contained at least one pesticide residue. The most frequently detected pesticide was bifenthrin with detection rates of 61.6%. Risk assessment was performed using both the deterministic approach and semiprobabilistic model under the best‐case and the worst‐case scenarios. The results demonstrated that the dietary risks were extremely low for six different subpopulations in which the risks for adults over the age of 41 were relatively higher. The risk ranking scheme indicated that isocarbophos and triazophos were considered to be of medium risk. The different use suggestions for the 25 positive pesticides are proposed to further minimize the exposure risk to consumer health. Practical Application: Tea is the second most popular nonalcoholic beverage throughout the world. Pesticides are used to improve the yield of tea. Pesticide residues in tea could be one of the exposure pathways for consumers. Monitoring residual levels and assessing the health risk assessment in tea are thus in an urge. [ABSTRACT FROM AUTHOR]

To assess the dietary exposure risks of pesticide residues in snow fungus for the general population and young children, 91 snow fungus samples were collected from major production areas in Fujian Province, China and the presence of 44 pesticides was determined. A total of thirteen pesticides were detected; 65.9% of the samples contained one or more pesticide residues. The most frequently found pesticide was carbofuran, followed by acetamiprid and then imidacloprid. Data obtained were used for chronic, acute, and chronic cumulative dietary exposure risk assessments. The chronic hazard quotient (cHQ) was extremely low for both the general population and young children. The %ADI values of cumulative dietary exposures to organophosphorus pesticides and carbamates ranged from 0.53% to 1.49%, and did not exceed their corresponding ADIs. However, the acute dietary risks from all 13 pesticides, especially carbofuran and methamidophos, were of concern due to the relatively high acute hazard quotient. The risk ranking scheme showed that carbofuran could pose a high risk to snow fungus consumers. Finally, suggestions are made about the potential use in snow fungus cultivation of the pesticides with detected residues. [ABSTRACT FROM AUTHOR]

To assess the health risks from antibiotic residues in freshwater fish, this study analyzed residues of 65 antibiotics in 10 freshwater fish species sampled in southeast China. Eight antibiotics were detected by UPLC-MS/MS at an overall detection rate of 53.9 %, with 3.48 % of samples exceeding MRLs and 13.0 % suggesting the misuse of human antibiotics. Quinolones, particularly enrofloxacin, were the most frequently detected residues. Azithromycin, an antibiotic intended only for human use, was detected at a rate of 14.8 % at concentrations up to 453.1 µg/kg. Antibiotic residues varied in category and concentration across freshwater fish species. Residues were detected in benthic predatory fish at higher levels than in middle or upper omnivorous or herbivorous fish. Estimated daily intakes showed that the consumption of cultured fish from this region does not pose a serious risk to human health, the hazard index being less than one. However, these findings suggest that the abuse of antibiotics in aquaculture is still a problem, and more attention should be paid to their residues in fish to enhance food safety. • Multi-residue method developed and validated for 65 antibiotics in freshwater fish. • Quinolones, particularly enrofloxacin, were the most abundant residues. • More residues in benthic predatory fish than middle/upper omnivorous/herbivorous fish. [ABSTRACT FROM AUTHOR]

Highlights: [•] Doxorubicin induces the down-expression of HDAC1 to exacerbate DNA damage. [•] Doxorubicin specifically downregulate the expression of HDAC1 but not other HDACs. [•] HDAC1 is a target of miR-520h which was upregulated after doxorubicin treatment. [•] The effect of doxorubicin was impaired by exogenous HDAC1 or miR-520h inhibitors. [•] HDAC1 reduced γH2AX by interfering the interaction of doxorubicin with genomic DNA. [Copyright &y& Elsevier]

Background: The role of Berberine (BBR) in colorectal cancer (CRC) and gut microbiota has begun to appreciate. However, there was no direct evidence confirm that the gut microbiota regulated by BBR could inhibit CRC. This report investigated the effect of stool from BBR treated subjects and its effect on CRC.Methods: A mouse model for CRC was developed using azoxymethane (AOM) and dextran sulfate sodium (DSS). Intestinal tissue from affected mice were used to determine the efficacy of BBR against CRC. Stool samples were collected for the 16s rRNA gene sequencing and fecal microbiota transplantation (FMT). Finally, the mechanism of gut microbiota from BBR treated mice on CRC was explored using immunohistochemistry, RNA-Sequencing, quantitative RT-PCR, and western blot analyses.Results: BBR significantly reduced intestinal tumor development. The richness of gut microbiota were notably decreased by BBR. Specifically, the relative abundance of beneficial bacteria (Roseburia, Eubacterium, Ruminococcaceae, and Firmicutes_unclassified) was increased while the level of bacteria (Odoribacter, Muribaculum, Mucispirillum, and Parasutterella) was decreased by BBR treatment. FMT experiment determined that the mice fed with stool from BBR treated AOM/DSS mice demonstrated a relatively lower abundance of macroscopic polyps and a significantly lower expression of β-catenin, and PCNA in intestinal tissue than mice fed with stool from AOM/DSS mice. Mechanistically, intestinal tissue obtained from mice fed with stool from BBR treated AOM/DSS mice demonstrated a decreased expression of inflammatory cytokines including interleukin 1β (IL-1β), tumor necrosis factor-α (TNF-α), C-C motif chemokine 1 (Ccl1), Ccl6, and C-X-C motif ligand (Cxcl9). In addition, the NF-κB expression was greatly suppressed in mice fed with stool from BBR treated AOM/DSS mice. Real-time PCR arrays revealed a down-regulation of genes involved in cell proliferation, angiogenesis, invasiveness, and metastasis in mice fed with stool from BBR treated AOM/DSS mice.Conclusions: Stool obtained from BBR treated AOM/DSS mice was able to increase colon length while simultaneously decreasing the density of macroscopic polyps, cell proliferation, inflammatory modulators and the expression of NF-κB. Therefore, it was concluded that suppression of pro-inflammatory genes and carcinogens factors by modulating gut microbiota was an important pathway for BBR to inhibit tumor growth in conventional mice. [ABSTRACT FROM AUTHOR]

Background. Curcumin is a polyphenol plant-derived compound with anti-inflammatory, antioxidant stress, and anticancer properties that make it have the potential to treat cancer cachexia. However, the role of it in breast cancer cachexia remains unclear. Methods. The 4T1 cells were subcutaneously injected into BALB/c mice to induce breast cancer cachexia. After tumor formation, the animals were divided into groups and given curcumin or saline interventions. The therapeutic effect of curcumin on breast cancer cachexia was characterized by tumor growth, changes in body mass and gastrocnemius mass, muscle function test, histopathology, and serum nutrition indexes. Mitochondrial function in muscle tissue was observed by transmission electron microscopy and ATP detection, muscle inflammatory factors were detected by ELISA, muscle differential metabolites were detected by 1HNMR metabolomics, and the muscle tissue ubiquitination levels and NF-KB expression were also analyzed by RT-qPCR and Western blot. Results. Dynamic in vivo bioluminescence imaging find that curcumin inhibited the growth of tumor in triple-negative breast cancer- (TNBC-) bearing mice, slowed down the loss of body weight and gastrocnemius weight, corrected the mitochondrial dysfunction and malnutrition status, and also significantly improved skeletal muscle function. ELISA analysis found that the level of inflammatory factors in muscle tissue was reduced. 1HNMR metabolomics analysis suggested that curcumin could regulate energy metabolism pathways. RT-qPCR and Western blot analysis found that the expression of myogenic factor myogenin was increased and the expression of myodegradation factor myostatin was decreased in the gastrocnemius; the level of ubiquitination and activation of the NF-κB pathway were also declined. Conclusions. Curcumin reduces ubiquitination, inflammation in skeletal muscle by regulating the NF-KB/UPS axis and improves muscle malignant metabolic phenotype and mitochondrial dysfunction, to alleviate muscle atrophy and loss of function in mice with breast cancer cachexia. [ABSTRACT FROM AUTHOR]

Purpose: We aim to investigate the role of Golgi phosphoprotein 3 (GOLPH3) and the possible regulation mechanism underlying lung adenocarcinoma (LADC). Methods: The level of GOLPH3 was performed by quantitative real time (qRT)-PCR, Western blot and immunohistochemistry. Patient survival rate was analyzed by Kaplan–Meier method. MTT was used to detect cell viability. The levels of p-serine/threonine-protein kinase (Akt), Akt, p-p65, p65 and β-catenin were determined by Western blot. Cell apoptosis was tested using flow cytometry. Angiogenesis was determined by in vitro angiogenesis assay. qPCR and Western blot were performed to identify apoptotic protein B-cell lymphoma 2 (Bcl-2)/Bcl-2-associated X protein (Bax) and vascular endothelial growth factor (VEGF). Results: GOLPH3 was highly expressed in LADC cell lines and tissues and was significantly correlated with poor overall survival among patients with LADC. Furthermore, GOLPH3 expression was reduced in A549 and H23 cells in a cisplatin-dependent manner. Silencing of GOLPH3 enhanced inhibition of A549 and H23 cells by cisplatin and suppressed the protein expression of p-Akt, while p-p65 expression remained stable. However, overexpression of GOLPH3 weakened the inhibition of A549 and H23 cells by cisplatin and improved the protein expression of p-Akt, while p-p65 expression remained stable. XAV939, an inhibitor of Wnt/β-catenin signaling pathway, decreased GOLPH3 overexpression-induced proliferation and enhanced cisplatin-induced angiogenesis inhibition and apoptosis, which was supported by the changes of VEGF, Bax and Bcl-2. Conclusion: GOLPH3 promotes proliferation capacity in LADC through activating the Wnt/β-catenin signaling pathway. [ABSTRACT FROM AUTHOR]

Background: Malnutrition is a common clinical symptom in cancer patients after chemotherapy, which is characterized by muscle wasting and metabolic dysregulation. The regulation of muscle metabolism by gut microbiota has been studied recently. However, there is no direct convincing evidence proving that manipulating gut microbiota homeostasis could regulate muscle metabolic disorder caused by chemotherapy. Here, we investigate the potential role of gut microbiota in the regulation of the muscle metabolism in 5-fluorouracil (5-Fu)-induced malnutrition rat model.Methods: Male Sprague-Dawley rats were randomly divided into two groups (n = 8/group): control group and 5-Fu group. In the 5-Fu group, rats received 5-Fu (40 mg/kg/day) by intraperitoneal injection for 4 days, and all rats were raised for 8 days. Nutritional status, muscle function, muscle metabolites, and gut microbiota were assessed. Fecal microbiota transplantation (FMT) was applied to explore the potential regulation of gut microbiota on muscle metabolism.Results: 5-Fu-treated rats exhibited loss of body weight and food intake compared to control group. 5-Fu decreased the levels of total protein and albumin in serum, and significantly increased the levels of IL-6 and TNF-α in muscle tissue. Rats that received 5-Fu displayed concurrent reduction of muscle function and fiber size. Moreover, 5-Fu group showed a distinct profile of gut microbiota compared to control group, including the relative lower abundance of Firmicutes and a higher abundance of Proteobacteria and Verrucomicrobia. Fourteen differential muscle metabolites were identified between two groups, which were mainly related to glycolysis, amino acid metabolism, and TCA cycle pathway. Furthermore, fecal transplantation from healthy rats improved nutritional status and muscle function in 5-Fu-treated rats. Notably, FMT inhibited the inflammatory response in muscle, and reversed the changes of several differential muscle metabolites and energy metabolism in 5-Fu-treated rats.Conclusions: Our study demonstrated that gut microbiota played an important role in the regulation of muscle metabolism and promoting muscle energy production in 5-Fu-induced malnutrition rats, suggesting the potential attenuation of chemotherapy-induced muscle wasting by manipulating gut microbiota homeostasis. [ABSTRACT FROM AUTHOR]

Aims Colorectal cancer threatens human health due to its high mortality resulting from metastatic progression. The expression of C-X-C chemokine receptor type 4 (CXCR4) is absent or low in most healthy tissues but high in various types of tumours. In this study, we aim to determine the prognostic significance of CXCR4 in colorectal cancer. Main methods We retrospectively examined a total of 72 tissue samples, that qRT-PCR and immunohistochemistry were performed to detect the expression of CXCR4 as well as univariate and multivariate analyses were performed to explore the overall survival. Key findings Our data demonstrated that CXCR4 expression was associated with lymph node metastasis ( P  = 0.049), histological differentiation ( P  = 0.01), distant metastasis ( P  = 0.02) and DNA mismatch repair (MMR) index ( P  = 0.0002). However, CXCR4 expression was not associated with age, sex, tumour diameter or depth of invasion. Furthermore, both univariate and multivariate analyses confirmed that CXCR4 was an independent factor in predicting unfavourable overall survival (hazard ratio, 0.188; 95% confidence interval, 0.038–0.757). Significance In conclusion, our findings suggest that CXCR4 might contribute to clinical tumour progression and may be a valuable prognostic biomarker in colorectal cancer treatment. [ABSTRACT FROM AUTHOR]

Under pathological conditions, the Janus kinase (JAK)/STAT signaling pathway can regulate the proliferation, differentiation and migration of tumor cells, including colorectal cancer (CRC). CRC is the third major types of cancer among males and the second among females worldwide. In China, CRC is the fifth common cancer among both males and females. Western blotting, flow cytometry, RNA interference, immunoprecipitation, xenografts models, and immunohistochemical staining were carried out to evaluate the possible mechanisms of acton of ruxolitinib. The present data suggested that ruxolitinib can suppress CRC cell proliferation by inducing apoptosis. Firstly, JAK1/2-STAT1 was identified as the target of ruxolitinib. Then, ruxolitinib downregulated myeloid cell leukemia-1 (Mcl-1) mRNA level and decreased its protein level, which enabled Bak to trigger CRC apoptosis. Furthermore, ruxolitinib exerted potent activity against CRC xenograft growth in vivo. High expression of phosphorylated STAT1 (S727) was also confirmed in 44 pairs of human colon carcinoma and adjacent normal tissues. Taken together, the results showed that ruxolitinib decreased JAK1/2-STAT1-Mcl-1 protein level and effectively suppressed CRC cell proliferation in vitro and in vivo. Therefore, ruxolitinib could be a promising anticancer agent for CRC treatment. [ABSTRACT FROM AUTHOR]

Curcumin up-regulated the expression of TET1, which could also be promoted by its transcriptional mediator Pax-6 and in turns induced the expression of NKD2. The WNT signal pathway was inhibited by the high expressed NKD2 and EMT progress was suppressed. As a result, the migration and invasion of 5-FU resistance HCT-116 cells were inhibited. The present study claimed a possible signal pathway mechanism explaining the anti-resistant effects of curcumin against 5-FU resistance HCT-116 cells. • Curcumin enhanced the inhibitory effects of 5-FU against the cell growth of 5-FU resistant HCT-116 cells. • WNT signal pathway in resistant HCT-116 cells was significantly inhibited by curcumin. • We supposed that curcumin and Pax-6 might exert the same function on TET1. Colorectal cancer is a kind of gastrointestinal tumor with rising morbidity and mortality. 5-fluorouracil is one of the most effective chemotherapy drugs for the treatment of CRC. However, clinical data reported dramatic resistance on the treatment for CRC with 5-fluorouracil. Present study aims to explore the anti-resistant effect of curcumin and its mechanism. MTT assay was used to evaluate the proliferation of rHCT-116 cells. Flow cytometry was used to determine the apoptosis and cell cycle of rHCT-116 cells. Western Blot was performed to detect the expression level of TET1, NKD2, E-cadherin, Vimentin, β-catenin, TCF4 and Axin in transfected rHCT-116 cells. 5-fluorouracil resistant HCT-116 cells were successfully established. Curcumin was found to be effective in the inhibition of proliferation, inducement of apoptosis and block of G0/G1 phase on 5-fluorouracil treated HCT-116 cells. The expression of TET1 and NKD2 was greatly inhibited by high dosage of curcumin. The WNT signal pathway and EMT progress were suppressed in rHCT-116 cells by high dosage of curcumin. The inhibitory effects of curcumin on WNT signal pathway and EMT progress were verified to be consistent with Pax-6, TET1 and NKD2. Curcumin might exert anti-resistant effect of 5-FU on HCT-116 cells by regulating the TET1-NKD2-WNT signal pathway to inhibit the EMT progress. [ABSTRACT FROM AUTHOR]

Berberine (BBR) is an isoquinoline alkaloid, which has been used in the treatment of intestinal mucositis. However, BBR on chemotherapy-induced mucositis in cancer patients remains largely unknown. Here, we investigated the effect of BBR on intestinal mucositis induced by 5-fluorouracil (5-Fu) using rat model. We detected the degree of intestinal mucosal damage and inflammatory response in 5-Fu treated rats with or without BBR administration, and investigated the changes of fecal metabolites and gut microbiota using 1H NMR spectroscopy and 16S rRNA. The mechanism was further explored by fecal microbiota transplantation (FMT). Results showed that BBR treated rats displayed less weight loss, lower diarrhea score and longer colon length in 5-Fu treated rats. Meanwhile, BBR treatment significantly increased the expression of Occludin in ileum and decreased the d -lactate content in serum. Moreover, the expression of IL-1β, IL-6 and TNF-α in ileum were suppressed by BBR treatment. The pattern of fecal metabolism changed obviously after treated with 5-Fu, which was reversed by BBR. Importantly, BBR significantly increased the levels of butyrate and glutamine in feces from 5-Fu treated rats. In terms of gut microbiota, BBR enriched the relative abundance of Firmicutes and decreased Proteobacteria at the phylum level. Meanwhile, BBR increased the propotion of unclassified_f_ Porphyromonadaceae , unclassified_f_ Lachnospiraceae , Lactobacillus , unclassified_o_ Clostridiales , Ruminococcus , Prevotella , Clostridium IV , and decreased Escherichia/Shigella at the genera level. Furthermore, principal component analysis (PCA) showed that fecal transplantation led to changes in fecal metabolites. Fecal transplantation from BBR treated rats had low diarrhea score, reduced inflammatory response in ileum, and relieved intestinal mucosal injury, which may be caused by the increased of butyrate level in fecal metabolites. In conclusion, our study provides evidence that BBR regulates fecal metabolites to ameliorate 5-Fu induced intestinal mucositis by modifying gut microbiota. [ABSTRACT FROM AUTHOR]

Reactive oxygen species (ROS) are implicated in carcinogenesis, and cellular antioxidant systems are important for detoxifying ROS and reversing oxidant-mediated modifications. Glutathione S-transferase mu (GSTM) belongs to a family of phase II detoxification enzymes that catalyze the conjugation of reduced glutathione (GSH) to a wide range of endogenous and exogenous electrophilic compounds. The genotype of GSTM1 was associated with the risk and prognosis of cancer in several meta-analyses. This study explored the function of GSTM1 in hepatocellular carcinoma (HCC). Polymerase chain reaction (PCR) and western blotting (WB) were used to detect the levels of gene and protein expression. MTS assays, Transwell assays, and flow cytometry were used to explore the function of GSTM1 in vitro. The xenograft assay and tail vein injection model were used to explore the function of GSTM1 in vivo. The mRNA and protein expression of GSTM1 was downregulated in HCC, but the expression levels of GSTM1 were not correlated with patient survival time. In vitro , Transwell and doxorubicin (DOX)-induced apoptosis assays revealed that GSTM1 showed opposite functions in different HCC cell lines with varied TP53 genotype statuses. The overexpression of GSTM1 in the above cell lines led to a significant decrease in ROS and an increase in GSH concentration and TP53 levels, suggesting that the controversial role of GSTM1 resulted from the TP53 genotype of HCC cells. The overexpression of GSTM1 promoted cell migration and inhibited apoptosis in the MHCC-97H cell line (TP53 , R249S), but inhibited cell migration and increased apoptosis in the SMMC-7721 cell line (TP53 wildtype). GSTM1 down-regulation may partially account for ROS-mediated oxidative damage and HCC carcinogenesis. GSTM1 also regulates tumor progression by disrupting the ROS- TP53 axis in HCC cells with different genetic backgrounds. [ABSTRACT FROM AUTHOR]