Mechanistic insights into anti-cancer properties of Curcumin and Andrographis in colorectal cancer
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PROVIDER: PRJNA925203 | ENA |
REPOSITORIES: ENA
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Project description:Colorectal cancer (CRC) remains the major leading cause of cancer-related deaths worldwide. The limitations of current chemotherapeutic drugs in CRC include their toxicity, side effects, and exorbitant costs. To assess these unmet needs in CRC treatment, several naturally occurring compounds, including Curcumin and Andrographis, have gained increasing attention due to their multi-targeted functionality and safety vs. conventional drugs. In the current study, we revealed that a combination of Curcumin and Andrographis exhibited superior anti-tumor effects by inhibiting cell proliferation, invasion, colony formation, and induction of apoptosis. Genomewide transcriptomic expression profiling analysis revealed that Curcumin and Andrographis activated the ferroptosis pathway.
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Project description:Andrographis paniculata Nees and its major compound andrographolide is known to exhibit a pleothera of activities. Active component enriched extracts are known to provide various beneficial effects, and therefore it was interesting to investigate whether increased amount of major compound alters gene expression. To acheive this, HePG2 cells treated with Andrographis paniculata extract (AP) and andrographolide enriched –extract (AP20) were subjected to microarray analysis to check their effect on global gene expression.
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Project description:To investigate the effect of curcumin on the proliferation and migration of colon cancer cells, we used curcumin treated with HCT116 cells We then performed gene expression profiling using RNA-seq data from HCT116 cells.
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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:Mechanistic insights into anti-cancer properties of oligomeric proanthocyanidins from grape seeds in colorectal cancer
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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:Cervical cancer is the second most common cancer in women worldwide. In addition to the important role played by HPV, the underlying mechanism promoting cervical tumorigenesis is complex and involves deregulation of key signaling pathways. Recently, role of miRNA mediated abnormal regulatory mechanisms is implicated in the pathogenesis of cervical cancer. Micro RNAs are regulatory, non‐coding RNAs about 21–23 nucleotides in length and effects the expression of a number of genes at the post‐transcriptional level. For the past few decades, role of curcumin in inhibiting the growth of cervical cancer and increasing the chemo and radio- sensistivity has been studied extensively. Interestingly, curcumin was shown to downregulate NF-κB, Wnt/β-catenin, TGF‐β and various other signaling pathways in cervical cancer cells. Although, a number of microarray studies have examined the use of miRNAs as cancer diagnostic markers, the regulation of miRNAs upon treatment with curcumin in cervical cancer cells has not been studied. The current study is aimed to perform miRNA profiling in cervical cancer cells following curcumin treatment and to study the role of miRNAs in regulating the different signaling pathways.
2022-06-30 | GSE134723 | GEO
Project description:Curcumin, derived from the rhizome of Curcuma longa is a natural anti-cancer agent and has been shown to inhibit proliferation and survival of tumor cells. Although the anti-cancer effects of curcumin are well established, detailed understanding of the signaling pathways altered by curcumin is still unclear. In this study, we carried out SILAC-based quantitative proteomic analysis of CAL 27 cell line, a HNSCC cell line to investigate tyrosine signaling in response to curcumin. Using high resolution Orbitrap Fusion™ Tribrid™ Fourier transform mass spectrometer, we identified 627 phosphotyrosine sites mapping to 357 proteins. We observed alterations in the level of phosphorylation of 307 sites corresponding to 204 proteins upon curcumin treatment.
2018-10-24 | PXD002097 | Pride
Project description:Andrographis paniculata callus transcriptomes
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