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Background Right-sided colorectal cancer (RCRC) and left-sided colorectal cancer (LCRC) harbor different genetic alterations associated with immune response. Objective This study aimed to analyze the differences in T cell immune-related RNA expression patterns between RCRC and LCRC. Methods The differentially expressed genes (DEGs) and lncRNAs (DElncRNAs) between LCRC and RCRC were screened from the Cancer Genome Atlas (TCGA) database. A correlation analysis between DEGs or DElncRNAs and differential T cells was also performed to obtain T cell-related genes, followed by miRNA prediction. The mRNA-lncRNA network and the competitive endogenous RNA (ceRNA) network were subsequently constructed, and the expression level of mRNA in the ceRNA network was verified using GSE104645. Results RCRC patients had a poorer prognosis and were older than LCRC patients. In total, 923 DEGs and 328 DElncRNAs were screened between LCRC and RCRC patients. Compared to RCRC patients, LCRC patients showed a decrease in CD8+ T cells. In addition, 26 miRNAs, 8 mRNAs, and 10 lncRNAs were included in the ceRNA network. Finally, the validation analysis revealed that CDHR1 and PRLR were significantly downregulated, while TRIB2 was upregulated in RCRC patients compared to LCRC patients. Conclusion The analysis of T cell immune-related RNA expression might provide new insights into the underlying molecular mechanisms of the differences between LCRC and RCRC.

Objective. Rap1GAP is considered a tumor suppressor gene, but its regulatory mechanism in papillary thyroid cancer (PTC) has not been clearly elucidated. The aim of this study was to explore whether the regulation between Rap1GAP and sodium/iodine transporter (NIS) in tumorigenesis of PTC is mediated by TGF-β1. Methods. Western blotting (WB) and quantitative reverse-transcription polymerase chain reaction were performed to analyze the relationships between TGF-β1 concentration and NIS expression. After transfecting BCPAP cells with siRNAs, the Rap1GAP interference model was successfully established. Then, the expression and nuclear localization of TGF-β1 and pathway-related proteins were detected. Flow cytometry was applied to analyze cell apoptosis and cycle. WB was performed to detect apoptotic-related proteins. Wound healing and transwell assays were used to measure cell migration and invasion. EDU was performed to detect cell proliferative activity. Results. The results suggested that TGF-β1 could significantly inhibit the expression of NIS in both mRNA and protein levels. In BCPAP cells transfected with siRNA-Rap1GAP, the expression levels of TGF-β1, Foxp3, and p-Smad3 were significantly increased. By applying immunofluorescence assay, the nuclear localizations of TβR-1 and p-Smad3 were found to be activated. Moreover, anti-TGF-β1 can reverse the decrease in NIS expression caused by downregulation of Rap1GAP. Additionally, the knockdown of Rap1GAP could alter the cell apoptosis, cycle, migration, invasion, and proliferation of BCPAP. Conclusion. The downregulation of Rap1GAP expression can activate the TGF-β/Smad3 pathway to inhibit NIS expression and alter the tumor cell functions of PTC.

Background Pancreatic cancer remains one of the most lethal cancers. Objective This study aimed to analyze T cell-related biomarkers and their molecular network in pancreatic cancer. Methods RNAseq sequencing data and clinical data of pancreatic cancer were obtained from TCGA database. The STromal and Immune cells in MAlignant Tumours using Expression data (ESTIMATE) algorithm was used to screen the DEGs related to the tumor immune cells. The pearson correlation analysis were used to analyze the relationships between DEGs and T cells. Additionally, the T cell-related DEGs were subjected to protein-protein interaction, competing endogenous RNA (ceRNA), and chemical small molecule-target network construction. Furthermore, the prognosis-associated DEGs were screened. Results A total of 412 stromal score-associated and 312 immune score-associated DEGs were obtained. From these DEGs, 50 CD4+ T cell-related genes and 13 CD8+ T cell-related genes were selected. The PPI networks associated with immune cell-related genes were constructed and found that CD22, SELL, and OLR1 had higher degrees in the PPI network. The number of ceRNA regulatory relation pairs obtained from CD4+ T cells and CD8+ T cells were 59 and 48, respectively. Additionally, both CD4+ T cell- and CD8+ T cell-related genes predicted 29 small molecules. CXCL9 and GIMAP7 were screened out from CD4+ T cell-related genes, which were related with the survival of pancreatic cancer. Conclusion We mapped T cell-related gene profile in pancreatic cancer and constructed their potential regulatory network.

The aim of this study was to investigate the genes associated with ferroptosis and the progression of hepatocellular carcinoma (HCC). The RNA sequencing data of erastin-induced ferroptosis in HCC cells were downloaded from the Sequence Read Archive database with accession number SRP119173. The microarray dataset GSE89377 of HCC progression was downloaded from the Gene Expression Omnibus database. The ferroptosis-related genes were screened by differential analysis and HCC progression-related genes were screened by cluster analysis using Mfuzz. Then, the genes associated with ferroptosis and HCC progression were screened by Venn analysis, followed by functional enrichment, protein-protein interaction (PPI) analysis, and transcription factor (TF) prediction. Finally, survival analysis was performed using data from the Cancer Genome Atlas database. A total of 33 upregulated and 52 downregulated genes associated with HCC progression and ferroptosis were obtained, and these genes were significantly involved in the negative regulation of ERK1 and ERK2 cascades; the NAD biosynthetic process; alanine, aspartate, and glutamate metabolism; and other pathways. The PPI network contained 52 genes and 78 interactions, of which, cell division cycle 20 (CDC20) and heat shock protein family B (small) member 1 (HSPB1) were hub genes found in higher degrees. Among the 85 genes associated with HCC progression and ferroptosis, two TFs (activating TF 3 (ATF3) and HLF) were predicted, with HSPB1 targeted by ATF3. In addition, 26 genes that were found to be significantly correlated with the overall survival of HCC patients were screened, including CDC20 and thyroid hormone receptor interactor 13. Several genes associated with HCC progression and ferroptosis were screened based on a comprehensive bioinformatics analysis. These genes played roles in HCC progression and ferroptosis via the negative regulation of the ERK1 and ERK2 cascades; the NAD biosynthetic process; and alanine, aspartate, and glutamate metabolism. ATF3 and HSPB1 played important roles in HCC progression and ferroptosis, with HSPB1 possibly regulated by ATF3.

Increasing evidence suggested that cholesterol is an important integrant of cell membranes, that plays a key role in tumor progression, immune dysregulation, and pathological changes in epigenetic mechanisms. Based on these theories, there is a growing interest on targeting cholesterol in the treatment of cancer. Here, we comprehensively reviewed the major function of cholesterol on oncogenicity, the therapeutic targets of cholesterol and its metabolites in cancer, and provide detailed insight into the essential roles of cholesterol in mediating immune and epigenetic mechanisms of the tumor microenvironment. It is also worth mentioning that the gut microbiome is an indispensable component of cancer mediation because of its role in cholesterol metabolism. Finally, we summarized recent studies on the potential targets of cholesterol and their metabolism, to provide more therapeutic interventions in oncology.

Recent studies have shown that the short-chain fatty acids (SCFAs) produced by the gut microbiota play a positive role in the development of colorectal cancer (CRC). This study aims to elucidate the “food-microorganism-SCFAs” axis and to provide guidance for prevention and intervention in CRC. The PubMed, Embase and Cochrane databases were searched from their inceptions to August 2018, and 75 articles and 25 conference abstracts were included and analysed after identification and screening. The concentrations of SCFAs in CRC patients and individuals with a high risk of CRC were higher than those in healthy individuals. The protective mechanism of SCFAs against CRC has been described in three aspects: epigenetics, immunology and molecular signalling pathways. Many food and plant extracts that were fermented by microorganisms produced SCFAs that play positive roles with preventive and therapeutic effects on CRC. The “food-microorganism-SCFAs” axis was constructed by summarizing the pertinent literature. This study provides insight into the basic research and practical application of SCFAs by assessing the protective effect of SCFAs on CRC.

Oxaliplatin resistance reduces the efficacy of chemotherapy for colorectal cancer (CRC). This study aimed to screen molecular targets of oxaliplatin resistance in CRC to construct a ceRNA network. The differentially expressed mRNA and lncRNA between the oxaliplatin-resistant and oxaliplatin-sensitive colon cancer cell lines was determined using RNA sequencing data (no. GSE42387) from the NCBI GEO database. Gene Ontology BP (biological process) and KEGG pathway enrichment analyses were used to analyze the function and pathway enrichment of the differentially expressed mRNA and lncRNA. The lnCeDB and starBase v2.0 were used to predict miRNA, and Cytoscape software was used to build a ceRNA network. The top 5 mRNA, miRNAs, and lncRNAs with high degrees of connectivity in the ceRNA network were validated by qPCR. TCGA colon cancer clinical data was used to perform a survival analysis of patients with differential mRNA and lncRNA expression. Between the two groups, 2515 mRNAs and 23 lncRNAs were differentially expressed. We constructed a ceRNA network containing 503 lncRNA-miRNA-mRNA regulatory pairs, 210 lncRNA-miRNA pairs, 382 miRNA-mRNA pairs, and 212 mRNA co-expression pairs. The differentially expressed lncRNA, miRNA and mRNA were verified by qPCR. One lncRNA (HOTAIR) and 14 mRNAs significantly correlated with patient prognosis. The discovery of differentially expressed genes and the construction of ceRNA networks will provide important resources for the search for therapeutic targets of oxaliplatin resistance. Moreover, this resource will aid the discovery of the mechanisms behind this type of drug resistance.

Background Sodium butyrate (NaB) is produced through the fermentation of dietary fiber that is not absorbed and digested by the small intestine. Purpose Here, we aimed to investigate the effects of NaB on the proliferation, invasion, and metastasis of CRC cells and their potential underlying molecular mechanism(s). Methods The cell counting kit-8 (CCK-8) assay and EdU assay were used to detect cell proliferation ability, flow cytometry was used to investigate the induction of apoptosis and cell cycle progression, and the scratch-wound healing and transwell assays were used to evaluate cell migration and invasion, respectively. The human CRC genome information for tissues and CRC cells treated with NaB obtained from the NCBI GEO database was reannotated and used for differential RNA analysis. Functional and pathway enrichment analyses were performed for differentially expressed lncRNAs and mRNAs. A protein-protein interaction (PPI) network for the hub genes was constructed using the Cytoscape software. Targeted miRNAs were predicted based on the lnCeDB database, and a ceRNA network was constructed using the Cytoscape software. The Kaplan-Meier method was used to analyze patient prognosis using the clinical information and exon-seq data for CRC obtained from the Broad Institute’s GDAC Firehose platform. Results NaB decreased the proliferation ability of CRC cells in a dose- and time-dependent manner. The number of apoptotic CRC cells increased with the increase in NaB concentrations, and NaB induced a G1 phase block in CRC cells. Moreover, NaB suppressed the migratory and invasive capabilities of CRC cells. There were 666 differentially expressed mRNAs and 30 differentially expressed lncRNAs involved in the CRC inhibition by NaB. The PPI network and ceRNA network were constructed based on the differentially expressed mRNAs and lncRNAs. Three differentially expressed mRNAs, including HMGA2, LOXL2, and ST7, were significantly correlated with the prognosis of CRC. Conclusion NaB induces the apoptosis and inhibition of CRC cell proliferation, invasion, and metastasis by modulating complex molecular networks. RNA prediction and molecular network construction need to be the focus of further research in this direction.

Background Patients with colorectal cancer (CRC) are at risk of malnutrition. Gut microbes and microbial metabolites are involved in the initiation and development of CRC. Purpose To investigate serum protein levels in CRC patients and explore the role of gut microbes and microbial metabolites in CRCs complicated with different serum albumin levels. Methods Overall, 398 CRC patients and same number of healthy volunteers in Huzhou Central Hospital from January 2016 to December 2018 were recruited to compare serum protein levels. The serological indicators were detected by Abbott Automatic Biochemical Analyzer(HCHL-YQ-SH-01). A total of 30 and 56 stool samples from CRC patients were used to detect intestinal microbes and microbial metabolites, respectively. Bacterial 16S V3-V4 and fungal ITS ribosomal DNA genes were sequenced and gas chromatography/mass spectrometry (GC/MS) was performed to detect microbial metabolites. Results Some serum protein-related indicators in the CRC group were lower than those in the control group (p༜0.05). The total protein and albumin levels in colon cancer patients were lower than those in rectal cancer patients (p༜0.05). The higher abundance of Sutterella is correlated with lower serum albumin level in CRCs. There were statistically significant differences in the abundance of fungi including Agaricomycetes, Simplicillium, Sclerotiniaceae, and Exophiala among patients with different serum albumin levels. Multiple gut bacteria and fungi are closely related to serum albumin levels.We found some characteristic microbial metabolites in CRCs complicated with different serum protein levels. Conclusions The different serum albumin levels were associated with the gut microbes and microbial metabolites in CRCs. It may provide novel ideas for basic research and clinical application.

Background. Thyroid carcinoma (THCA) is one of the most common malignancies of the endocrine system, which is usually treated by surgery combined with iodine-131 (I131) radiotherapy. Aims. This study is aimed at exploring the potential targets of I131 radiotherapy in THCA. Methods. The RNA-sequencing data of THCA in The Cancer Genome Atlas database (including 568 THCA samples) was downloaded. The differentially expressed genes (DEGs) between the tumour samples whether or not subjected to I131 radiotherapy were identified using edgeR package. Using the WGCNA package, the module that was relevant with I131 radiotherapy was selected. The intersection genes of the hub module nodes and the DEGs were obtained as hub genes, followed by the function and pathway enrichment analyses using the clusterProfiler package. Moreover, the protein-protein interaction (PPI) network for the hub genes was constructed using Cytoscape software. In addition, more important hub genes were analysed with function mining using the GenCLiP2 online tool. The qPCR analysis was used to verify the mRNA expression of more important hub genes in THCA tissues. Results. There were 500 DEGs (167 upregulated and 333 downregulated) between the two groups. WGCNA analysis showed that the green module (428 nodes) exhibited the most significant correlation with I131 radiotherapy. A PPI network was built after the identification of 53 hub genes. In the PPI network, CDH5, KDR, CD34, FLT4, EMCN, FLT1, ROBO4, PTPRB, and CD93 exhibited higher degrees, which were mainly implicated in the vascular function. The relative expression of nine mRNAs in the THCA tissues treated with I131 was lower. Conclusion. I131 radiotherapy might exert therapeutic effects by targeting CDH5, KDR, CD34, FLT4, EMCN, FLT1, ROBO4, PTPRB, and CD93 in THCA patients.

Background The colorectum includes ascending colon, transverse colon, descending colon, sigmoid colon, and rectum. Different sites of colorectal cancer (CRC) are different in many aspects, including clinical symptoms, biological behaviour, and prognosis. Purpose This study aimed to analyse prognosis, genes, bacteria, fungi, and microbial metabolome in different sites of CRC. Methods The Surveillance, Epidemiology, and End Results (SEER) database and STAT were used to statistically describe and analyse the prognosis in different sites of CRC. RNA sequences of CRC from Broad Institute’s GDAC Firehose were re-annotated and reanalysed based on different sites using weighted gene co-expression network analysis (WGCNA). The Kaplan–Meier method was used to analyse the prognosis and Cytoscape was used to construct a drug-target network based on DGIdb databases. Bacterial 16S V3–V4 and fungal ITS V3–V4 ribosomal RNA genes of stool samples were sequenced. Gas chromatography/mass spectrometry (GS/MS) was performed to detect the microbial metabolites in stool samples. Bioinformatics analysis was performed to compare distinct gut microorganisms and microbial metabolites between rectal and sigmoid cancers. Results The prognosis in CRC with different sites is significantly different. The closer to the anus predicted longer survival time. The difference between genes and co-expression pairs in CRC with different sites were constructed. The relative abundance of 112 mRNAs and 26 lncRNAs correlated with the sites of CRC were listed. Nine differentially expressed genes at different sites of CRC were correlated with prognosis. A drug-gene interaction network contained 227 drug-gene pairs were built. The relative abundance of gut bacteria and gut fungus, and the content of microbe-related metabolites were statistically different between rectal and sigmoid cancers. Conclusions There are many differences in prognosis, genome, drug targets, gut microbiome, and microbial metabolome in different colorectal cancer sites. These findings may improve our understanding of the role of the CRC sites in personalized and precision medicine.

Background Globally, hepatocellular carcinoma (HCC) is the third leading cause of cancer-related death. Recently, many studies have demonstrated that small nucleolar RNA (snoRNA) was closely related to HCC. Objective To explore whether snoRNA can be used as a molecular target for HCC. Methods The PubMed, Embase, and Cochrane databases were searched for the published literatures related to snoRNA and HCC until August 12, 2019. After identification, screening, and verification, this study finally included 26 studies correlating small nucleolar RNA host gene (SNHG) and HCC, and 8 studies correlating snoRNA and HCC. Based on the collation of the relevant literature, the correlation network diagram between snoRNAs and HCC was constructed. Results The SNHGs, such as SNHG1, SNHG6, SNHG16, and SNHG20 can play varied roles in HCC through different regulatory mechanisms. These SNHGs can promote and inhibit tumorigenesis. SNORD76 can promote the proliferation of tumor tissues and cells in vitro through different pathways. SnoU2_19 and SNORD76 can function through the same pathway. SNHG3, SNHG20, SNHG6, SNORD76, and snoRA47 can modulate epithelial-mesenchymal transition (EMT) to regulate the development of HCC cell or tissue. SNHG16, SNORD76, and SnoU2_19 can regulate the development of HCC through Wnt/β-catenin signaling pathway. Conclusion snoRNA can regulate the occurrence of HCC by modulating multiple molecular signaling pathways. Hence, snoRNA can be a potential molecular target for HCC.

Biochar(BC)-supported nanoscaled zinc oxide (nZO) was encapsulated either with (nZORc/BC) or with no (nZOR/BC) sodium carboxymethyl cellulose (CMC). The X-ray diffraction and ultraviolet (UV)-visible-near infrared spectrophotometry revealed that nZO of 16, 10, and 20 nm with energy band gaps of 2.79, 3.68 and 2.62 eV were synthesized for nZOR/BC, nZORc/BC and nZO/BC, respectively. The Langmuir isotherm predicted saturated sorption of methylene blue (MB) was 17.01 g kg−1 for nZORc/BC, over 19 times greater than nZOR/BC and nZO/BC. Under UV irradiation, 10.9, 61.6, 83.1, and 41.6% of MB were degraded for nZORc/BC, nZO/BC, nZOR/BC and BC. The scavenging experiment revealed hydroxyl radical dominated CMC degradation. Exogenous CMC (2 g L−1) increased MB sorption from 10.6% to 73.1%, but decreased MB degradation from 80.7% to 41.1%, relative to nZOR/BC. Thus, CMC could increase MB sorption by electrostatic attraction and other possible mechanisms. The compromised MB degradation may be ascribed to reduced availability of hydroxyl and superoxide radicals to degrade MB, and increased band gap energy of ZnO.

An activated carbon (AC)-supported nanocomposite was prepared by precipitating β-FeOOH onto KOH activated soybean meal-derived biochar (SYBK). The as-prepared β-FeOOH/SYBK composites were characterized by N2-Brunauer–Emmett–Teller (BET), scanning electron microscopy (SEM), X-ray diffractions (XRD) and X-ray photoelectron spectroscopy (XPS). XRD results confirmed that β-FeOOH was impregnated by AC. The chromate (Cr(VI)) removal capacity was investigated in a batch experiment with different conditions. The ratios of β-FeOOH and AC were compared for Cr(VI) removal and a loading quantity of 20 wt% β-FeOOH was considered as the most efficient amount. This was possibly ascribed to it having the highest surface area (670.65 m2 g−1) of the β-FeOOH/SYBK nanocomposites. It was found that 20β-FeOOH/SYBK could remove as much as 96% Cr(VI) at pH 1–2 with 2 mmol L−1 EDTA and 2.0 g L−1 nanocomposites. The maximal Cr(VI) removal by 20β-FeOOH/SYBK was 37.04 g kg−1, as estimated by a Langmuir isotherm model. The removal mechanisms were examined by studying the speciation of Cr on sorbents as well as in aqueous solution. The XPS analysis of spent sorbents and chemical speciation of Cr in aqueous solutions revealed that partial Cr(VI) was reduced to Cr(III) on sorbents and in aqueous solution. This suggests that Cr(VI) can be removed by simultaneous sorption and reduction by the as-prepared nanocomposites.

Colorectal cancer (CRC) was one of the most frequent cancers worldwide. Accurate risk and prognosis evaluation could obtain better quality of life and longer survival time for the patients. Current research hotspot was focus on the gene biomarker to evaluate the risk and prognosis. Mitochondrion contains its own DNA and regulates self-replicating so that it can be as a candidate biomarker for evaluating the risk and prognosis of colorectal cancer. But there were already huge controversies on this issue. The review was to summarize current viewpoints of the controversial issues and described our understanding from the four aspects including mtDNA copy number, mitochondrial displacement loop, mtDNA variation, and mtDNA microsatellite instability, wishing the summary of the mtDNA in colorectal cancer could provide a meaningful reference or a valuable direction in the future studies.

Colorectal cancer (CRC) is a common type of malignant cancer worldwide. Recent studies have identified the gut microbiota as the origin of CRC, and T lymphocyte-mediated immune functions have been shown to play an important role in this disease. By summarizing previous literature, we found that Fusobacterium nucleatum may protect CRC from immune cell attack by inhibiting T cells and influencing the production of many chemokines and cytokines. Some bacterial metabolites and probiotics have been shown to participate in the regulation of CRC through T cell-mediated molecular pathways. To visualize the relevant data, an association network of intestinal microorganisms and T lymphocytes associated with CRC was constructed. This work may provide direction for – and insight into – further research on the relationship between intestinal microorganisms and T lymphocytes in CRC.

Background Chemotherapy induced diarrhea (CID) is a common side effect in patients receiving chemotherapy for cancer. The aim of our study was to explore the association between gut microorganisms and CID from the CapeOX regimen in resected stage III colorectal cancer (CRC) patients. Results After screening and identification, 17 stool samples were collected from resected stage III CRC patients undergoing the CapeOX regimen. Bacterial 16S ribosomal RNA genes was sequenced, and a bioinformatics analysis was executed to screen for the distinctive gut microbiome and the functional metabolism associated with CID due to the CapeOX regimen. The gut microbial community richness and community diversity were lower in CID (p 2), and there were 23 pathways that the differential microorganisms might be involved in. Conclusions The gut microbial community structure and diversity have changed in CRC patients with CID. It may provide novel insights into the prevention and treatment of CID. Electronic supplementary material The online version of this article (10.1186/s13099-019-0299-4) contains supplementary material, which is available to authorized users.

Colorectal cancer (CRC) is one of the most common malignancies worldwide and a major cause of cancer-related deaths. Numerous studies have suggested that piwi-interacting RNAs (piRNAs), a new type of non-coding RNA (ncRNA), are closely related to the occurrence and development of cancer. piRNAs have been shown to regulate the occurrence of CRC by modulating multiple molecular signaling pathways. Here, the roles of piRNAs in CRC were reviewed to provide evidence for their potential as molecular targets for CRC.

Background The gut microbiome changes are related to the colorectal cancer (CRC). Chemotherapy is one of the main treatment methods for CRC. Purpose To explore the effect of chemotherapy on the gut bacteria and fungi in CRC. Methods Total of 11 advanced CRC patients treated with the FOLFIRI regimen, 15 postoperative CRC patients treated with the XELOX regimen, and corresponding CRC patients without surgery and chemotherapy were recruited. The 16S ribosomal RNA and ITS sequences were sequenced, and bioinformatics analysis was executed to screen for the distinctive gut microbiome. Results The abundances of Veillonella, Humicola, Tremellomycetes and Malassezia were increased in postoperative CRC patients treated with the XELOX regimen. The abundances of Faecalibacterium, Clostridiales, phascolarctobacterium, Humicola and Rhodotorula were decreased, and the abundances of Candida, Magnusiomyces, Tremellomycetes, Dipodascaceae, Saccharomycetales, Malassezia and Lentinula were increased in advanced CRC patients treated with the FOLFIRI regimen. The abundances of Humicola, Rhodotorula, and Magnusiomyces were decreased, and the abundances of Candida, Tremellomycetes, Dipodascaceae, Saccharomycetales, Malassezia and Lentinula were increased in advanced CRC patients treated with the FOLFIRI regimen combined with cetuximab compared with those treated with the FOLFIRI regimen alone. Conclusions The community structure of gut bacteria and fungi changes in chemotherapy on CRCs.

In this study, the changes in the enzymatic activity and bacterial communities inhabiting the earthworm gut were investigated to determine the correlation between feeding conditions and tetracycline (TC) degradation. Two TC concentrations (high and low) were fed to earthworms using either the sequential swallowing or repeated swallowing technique. The repeated swallowing feeding technique was found to have a better effect on the degradation rate of TC. The peroxidase and catalase activities in earthworms fed using the sequential swallowing technique were higher than those in earthworms fed using the repeated swallowing technique. When the sequential swallowing technique was used, the TC degradation rate was found to be negatively correlated with the abundance of Clostridium, Hyphomicrobium, and Streptomyces, whereas when the repeated swallowing technique was used for feeding the earthworms, the TC degradation rate was positively correlated with the abundance of 18 bacterial species, including Clostridium, Hyphomicrobium, and Fodinicola.

Colorectal cancer is one of the most common malignant tumours. Competitive endogenous RNA (ceRNA) networks have been hypothesized, in which various RNAs regulate each other's expression using microRNA response elements (MREs). Recent evidence has highlighted the crucial regulatory roles of ceRNA networks in colorectal cancer. In this review, we summarize the present research methods as well as the currently known ceRNA competitors and targets in colorectal cancer. In addition, we discuss the significance of ceRNA and shortcomings of current studies of colorectal cancer.

Magnetic attapulgite-Fe3O4 nanocomposites (ATP-Fe3O4) were prepared by coprecipitation of Fe3O4 on ATP. The composites were characterized by scanning electron microscopey, X-ray diffractometry, Brunauer-Emmett-Teller analysis, X-ray photoelectron spectroscopy, energy dispersive spectrometer and transmission electron microscopy. Surface characterization showed that Fe3O4 particles with an average size of approximately 15 nm were successfully embedded in matrix of ATP. The capacity of the Fe3O4-activated ATP (A-ATP@Fe3O4) composites for catalytic degradation of ethidium bromide (EtBr, 80 mg/L) at different pH values, hydrogen peroxide (H2O2) concentrations, temperatures, and catalyst dosages was investigated. EtBr degradation kinetics studies indicated that the pseudo-first-order kinetic constant was 2.445 min−1 at T = 323 K and pH 2.0 with 30 mM H2O2, and 1.5 g/L of A-ATP@Fe3O4. Moreover, a regeneration study suggested that A-ATP@Fe3O4 maintained over 80% of its maximal EtBr degradation ability after five successive cycles. The effects of the iron concentrations and free radical scavengers on EtBr degradation were studied to reveal possible catalytic mechanisms of the A-ATP@Fe3O4 nanocomposites. Electron Paramagnetic Resonance revealed both hydroxyl (∙OH) and superoxide anion (∙O2−) radicals were involved in EtBr degradation. Radical scavenging experiment suggested EtBr degradation was mainly ascribed to ∙OH radicals, which was generated by reaction between Fe2+ and H2O2 on the surface of A-ATP@Fe3O4.