MiRNA expression profiling in cervical cancer cells following curcumin treatment
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE134723 | GEO | 2022/06/30
REPOSITORIES: GEO
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Project description:Inflammation is highly associated with colon carcinogenesis. Epigenetic mechanisms play an important role in the initiation and progression of colon cancer. Curcumin is a dietary cancer preventive phytochemical with promising effect in suppressing colitis-associated colon cancer (CAC) in azoxymethane (AOM) and dextran sulfate sodium (DSS) mouse model. In the present study, we confirmed the effect of curcumin in suppressing colon cancer. Using Agilent SureSelect Methyl-seq and RNA-seq, we obtained single-base methylation profile and transcriptome analyses of epithelial cells from control group, AOM and DSS induced group (AOM+DSS), and AOM and DSS induced plus curcumin treated group (AOM+DSS+Curcumin) in a 18 weeks long-term colon cancer mouse model. We observed differentially expressed genes in pair-wise comparison and identified several pathways of small set of genes involved in the potential preventive effect of curcumin. These pathways include LPS/IL-1 mediated inhibition of RXR function, NRF2-mediated oxidative stress response, aldosterone signaling in epithelial cells, production of NO and ROS in macrophages, and IL-6 signaling. The average DNA methylation levels of the three groups are significantly different also. Based on differential methylation patterns of three groups, several pathways of genes were identified including IL-8 signaling, LPS-stimulated MAPK signaling and colorectal cancer metastasis signaling. Among these methylated pathways and genes, Tnf, an inflammatory gene stood out with decreased DNA CpG methylation in the AOM-DSS as compared to the control group and interestingly curcumin reversed the CpG methylation (validated by pyrosequencing). These observations correlated with decreased, and increased with curcumin, Tnf expression in RNA-seq (validated by qPCR), respectively. The functional role of DNA methylation of Tnf was confirmed by in vitro luciferase transcriptional activity assay. In addition, we found that a group of genes associated with the inflammatory responses and their methylation level was decreased in AOM+DSS group but restored in the curcumin treated group. Taken together, in this study, aberrant DNA CpG methylation of the inflammatory response was found in colitis-associated colon cancer and curcumin restored their CpG methlyation, which could potentially explain the inflammatory and cancer protective effects of curcumin. (Note this GEO/dataset is the RNA-seq part of the study.)
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Project description:Curcumin is a polyphenolic compound extracted from the turmeric plant (Curcuma longa) and has been extensively studied for its anti-inflammatory and anti-proliferative properties. The safety and effectiveness of curcumin have been thoroughly proven. However, the mechanisms underlying the treatment of osteoarthritis remain unclear. This study aimed to reveal the potential mechanism of curcumin in the treatment of osteoarthritis through metabolomics and transcriptomics. First, we verified the effect of curcumin on inflammatory factors in human articular chondrocytes. Secondly, we used cellular metabolomics to explore the cellular metabolic mechanism of curcumin against osteoarthritis. Third, we evaluated differences in gene expression in human articular chondrocytes by transcriptomics. Finally, to evaluate essential targets and elucidate the underlying mechanisms of curcumin in the treatment of osteoarthritis, we performed a screen for proteins in pathways shared by metabolomics and transcriptomics. Our results showed that curcumin significantly reduced the levels of inflammatory markers, such as IL-β, IL-6, and TNF-α, in human articular chondrocytes. Cellular metabolomics identified 106 differential metabolites, including beta-aminopropionitrile, 3-amino-2-piperidone, pyrrole-2-carboxaldehyde, and various other components. Transcriptome analysis yielded 1050 differential mRNAs. Enrichment analysis showed that differential metabolites and mRNA were significantly enriched in 7 pathways including glycine, serine, and threonine metabolism; interconversion of pentose and glucuronic acid; glycerolipid metabolism; histidine metabolism; mucin type O-glycan biosynthesis; phosphoinositide metabolism; and cysteine and methionine metabolism. A total of 23 key targets were identified to be involved in these pathways. We speculate that curcumin may alleviate osteoarthritis by targeting key proteins involved in glycine, serine, and threonine metabolism, inhibiting pyruvate production, and regulating glycolysis.
2023-11-10 | GSE243421 | GEO
Project description:Inflammation is highly associated with colon carcinogenesis. Epigenetic mechanisms play an important role in the initiation and progression of colon cancer. Curcumin is a dietary cancer preventive phytochemical with promising effect in suppressing colitis-associated colon cancer (CAC) in azoxymethane (AOM) and dextran sulfate sodium (DSS) mouse model. In the present study, we confirmed the effect of curcumin in suppressing colon cancer. Using Agilent SureSelect Methyl-seq and RNA-seq, we obtained single-base methylation profile and transcriptome analyses of epithelial cells from control group, AOM and DSS induced group (AOM+DSS), and AOM and DSS induced plus curcumin treated group (AOM+DSS+Curcumin) in a 18 weeks long-term colon cancer mouse model. The average DNA methylation levels of the three groups are significantly different also. Based on differential methylation patterns of three groups, several pathways of genes were identified including IL-8 signaling, LPS-stimulated MAPK signaling and colorectal cancer metastasis signaling. Among these methylated pathways and genes, Tnf, an inflammatory gene stood out with decreased DNA CpG methylation in the AOM-DSS as compared to the control group and interestingly curcumin reversed the CpG methylation (validated by pyrosequencing). The functional role of DNA methylation of Tnf was confirmed by in vitro luciferase transcriptional activity assay. In addition, we found that a group of genes associated with the inflammatory responses and their methylation level was decreased in AOM+DSS group but restored in the curcumin treated group. Taken together, in this study, aberrant DNA CpG methylation of the inflammatory response was found in colitis-associated colon cancer and curcumin restored their CpG methlyation, which could potentially explain the inflammatory and cancer protective effects of curcumin. (Note this GEO/dataset is the DNA methyl-seq part of the study.)
2018-06-11 | GSE102645 | GEO
Project description:The cancer stem cells (CSCs) have important therapeutic implications for multi-resistant cancers including hepatocellular carcinoma (HCC). Among the key pathways frequently activated in liver CSCs is NF-kB signaling. Here we evaluated the CSCs-depleting potential of NF-kB inhibition in liver cancer achieved by IKK inhibitor curcumin and specific peptide SN50 . The effects on CSCs were assessed by analysis of Side Population (SP) and expression levels of CSC-related genes as determined by RT-qPCR, gene expression microarray, EMSA, and Western blotting. Curcumin caused anti-proliferative and pro-apoptotic responses directly related to the extent of NF-kB inhibition. In curcumin-sensitive tumor cells, the treatment led to a selective CSC depletion as evidenced by a reduced SP size, decreased sphere formation, down-regulation of CSC markers and suppressed tumorigenicity. Similarly, NF-kB inhibition by SN50 caused a general suppression of cell growth accompanied by a reduced SP fraction. In contrast, curcumin-resistant cells exhibited a paradoxical increase in proliferation and expression of CSC markers. Mechanistically, CSC-depleting activity of curcumin was exerted by the NF-kB-mediated HDAC inhibition causing down-regulation of c-MYC and other key oncogenic targets. Co-administration of the class I/II HDAC inhibitor trichostatine sensitized resistant cells to curcumin. Further, integration of a predictive signature of curcumin sensitity with our HCC database indicated that HCC patients with poor prognosis and progenitor features are most likely to benefit from NF-kB inhibition. These results demonstrate that NF-kB inhibition can specifically target CSC populations and suggest a potential for combined inhibition of NF-kB and HDAC signaling for treatment of liver cancer patients with poor prognosis. Five human hepatoma cell lines with and without curcumin
2015-12-31 | E-GEOD-59713 | biostudies-arrayexpress
Project description:Background Clinical practice demonstrates that anticancer drug effects may strongly vary between different patients. Individual responses to drug action are potentially responsible for adverse effects such as establishment of resistance. Consequently, the understanding of response mechanisms to drug actions is of great relevance. Proteome profiling is a powerful tool for the investigation of cellular responses to drugs. Methods Here, we have investigated the effects of curcumin, a natural remedy with known anti-cancer activities, on breast cancer cells MCF-7, ZR-75-1 and normal mammary fibroblasts as well as co-cultures thereof using proteome profiling. The mammary fibroblasts had been treated before with TGF-beta in order to induce a wound-healing signature known to be representative for the in vivo situation in breast tumors. Results While co-culture alone induced several proteins like ANXA1, S100A4 and SPARC similarly in both breast cancer cells, the majority of proteins regulated upon co-culture differed between MCF-7 and ZR-75-1. Curcumin significantly induced HMOX1 in all single cell models and co-cultures. However, otherwise the curcumin effects differed. In the MCF-7 co-culture, curcumin significantly downregulated RC3H1, a repressor of inflammatory signaling. In the ZR-75-1 co-culture, curcumin significantly downregulated PEG10, an anti-apoptotic protein, and induced RRAGA, a pro-apoptotic protein involved in TNF-alpha signaling. In this model, curcumin also induced AKR1C2, an important enzyme for progesterone metabolism. None of these specific curcumin effects were observed in single cell cultures. Conclusions The present data demonstrate that curcumin induces proteome alterations potentially accounting for its known antitumor effects in a strongly context-dependent fashion.
2018-06-04 | PXD008719 | Pride
Project description:The cancer stem cells (CSCs) have important therapeutic implications for multi-resistant cancers including hepatocellular carcinoma (HCC). Among the key pathways frequently activated in liver CSCs is NF-kB signaling. Here we evaluated the CSCs-depleting potential of NF-kB inhibition in liver cancer achieved by IKK inhibitor curcumin and specific peptide SN50 . The effects on CSCs were assessed by analysis of Side Population (SP) and expression levels of CSC-related genes as determined by RT-qPCR, gene expression microarray, EMSA, and Western blotting. Curcumin caused anti-proliferative and pro-apoptotic responses directly related to the extent of NF-kB inhibition. In curcumin-sensitive tumor cells, the treatment led to a selective CSC depletion as evidenced by a reduced SP size, decreased sphere formation, down-regulation of CSC markers and suppressed tumorigenicity. Similarly, NF-kB inhibition by SN50 caused a general suppression of cell growth accompanied by a reduced SP fraction. In contrast, curcumin-resistant cells exhibited a paradoxical increase in proliferation and expression of CSC markers. Mechanistically, CSC-depleting activity of curcumin was exerted by the NF-kB-mediated HDAC inhibition causing down-regulation of c-MYC and other key oncogenic targets. Co-administration of the class I/II HDAC inhibitor trichostatine sensitized resistant cells to curcumin. Further, integration of a predictive signature of curcumin sensitity with our HCC database indicated that HCC patients with poor prognosis and progenitor features are most likely to benefit from NF-kB inhibition. These results demonstrate that NF-kB inhibition can specifically target CSC populations and suggest a potential for combined inhibition of NF-kB and HDAC signaling for treatment of liver cancer patients with poor prognosis.
2015-12-31 | GSE59713 | GEO
Project description:Previous research reports have shown that curcumin and exercise have good anti-tumor effects. However, there is currently a lack of relevant research reports on the combined effect of physical exercise with curcumin supplementation on cancer and its mechanisms. This study constructed an anti breast tumor mouse model under the combined effects of curcumin treatment and swimming exercise. Transcriptomics and metabolomics techniques were used to screen differentially expressed genes and metabolites, evaluate the anti-cancer effect, and analyze the molecular regulatory mechanisms related to metabolism. Through the mouse phenotype observation, including the detection of tumor appearance, tumor imaging in vivo, and HE staining results of pathological sections, curcumin administration and exercise intervention combined treatment has more obvious inhibitory effect on breast cancer than a single treatment. The combined effect treatment group had a total of 445 differentially expressed genes, including 154 upregulated genes and 291 downregulated genes; Functional enrichment analysis showed that calcium signaling pathway, Wnt signaling pathway, PI3K Akt signaling pathway and IL-17 signaling pathway significantly participated in the anti breast cancer process of curcumin combined exercise. The results of inter group differential metabolite analysis showed that the combined effect of curcumin and exercise involves two unique pathways: amino sugar and nucleotide sugar metabolism, as well as amino acid biosynthesis. The metabolic pathways of amino sugars and nucleotide sugars include chitosan, D-glucosamine 6-phosphate, L-fucose, and N-acetyl beta-mannosamine; The biosynthetic pathway of amino acids includes DL isoleucine, DL tyrosine, and homocysteine. Finally, through the joint analysis of transcriptome and metabolomic data, it was found that the most significantly correlated genes among the positive ion mode differential metabolites under the combined exercise of curcumin were catechins, including 8 correlated genes Cpeb2, Grem1, Nid1, Samd5, Hsph1, Glis3, Mapk6, and Phldb2; The most significant negative ion mode differential metabolite is 1-myristyl-2-hydroxy-sn-glycerol-3-phosphate ethanolamine, which includes 27 correlated genes Mmp10, Dock4, Dpysl3, Tnfsfm13, Etf1, Dzip1, Scara5, Plcg2, Dusp18, Zmat3, Marf1, Tox4, Tmem119, Tep1, Cybc1, AW549877, Dynap, Hhip, Tpm3, Zc3hav1l, Sema5a, Txlng, Lrrc55, Pprrx1, Rtl8b, Adam19, and Frrs1.
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