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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Role of miR-19b and its target mRNAs on 5-fluorouracil resistance in colon cancer cells

ABSTRACT: Despite the efforts in defining the molecular mechanisms for the drug resistance in colorectal cancers, little is known about the roles of microRNAs. With microarray containing 723 microRNAs, we examined effect of 5-fluorouracil (5-FU) on the microRNA expression. Respond to 5-FU, we identify two microRNAs, miR-19b and miR-21, that were differentially expressed in 5-FU resistant colon cancer cells derived from KM12C and DLD-1. DLD-1, DLD-1/R, KM12C, and KM12C/R cells were plated at 1 × 105 cells/well. After pre-culture, cells were treated with 60 uM of 5-FU for 72 h. This was the same condition as the analysis of cell cycle. RNAs were collected before (0 h) and after the treatment of 5-FU (72 h).

ORGANISM(S): Homo sapiens

SUBMITTER: Toshihito Tanahashi

PROVIDER: E-GEOD-30894 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Role of miR-19b and its target mRNAs on 5-fluorouracil resistance in colon cancer cells

Project description:Despite the efforts in defining the molecular mechanisms for the drug resistance in colorectal cancers, little is known about the roles of microRNAs. With microarray containing 723 microRNAs, we examined effect of 5-fluorouracil (5-FU) on the microRNA expression. Respond to 5-FU, we identify two microRNAs, miR-19b and miR-21, that were differentially expressed in 5-FU resistant colon cancer cells derived from KM12C and DLD-1.

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miR-19b-3p Overexpression in Human Skeletal Muscle Cells

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Proteomic analysis upon miR195/497 replacement reveals potential chemo sensitizing candidates for colorectal cancer

Project description:Patients with advanced colorectal cancer (CRC) are commonly treated with systemic combination therapy but suffer eventually from drug resistance. MicroRNAs (miRNAs) are suggested to play a role in treatment resistance of CRC. We studied whether restoring downregulated miR-195-5p and 497-5p sensitize CRC cells to currently used chemotherapeutics 5-fluorouracil, oxaliplatin and irinotecan. Sensitivity to 5-FU, oxaliplatin and irinotecan before and after transfection with miR-195-5p and miR-497-5p mimics was analyzed in CRC cell lines HCT116, RKO, DLD-1 and SW480. Mass spectrometry based proteomic analysis of transfected and wild-type cells was used to identify targets involved in sensitivity to chemotherapy. Proteomic analysis revealed 181 proteins with significantly altered expression after transfection with miR-195-5p mimic in HCT116 and RKO, including 118 downregulated and 63 upregulated proteins. After transfection with miR-497-5p mimic, 130 proteins were significantly downregulated and 102 were upregulated in HCT116 and RKO (P<0.05 and FC<-3 or FC>3). CHUK and LUZP1 were coinciding downregulated proteins in sensitized CRC cells after transfection with either mimic. Resistance mechanisms of these two proteins may be related to nuclear factor kappa-B signaling and G1 cell cycle arrest, respectively. Restoring miR-195-5p and miR-497-5p expression enhanced sensitivity to chemotherapy, mainly oxaliplatin, in CRC cells and could be a promising treatment strategy for patients with mCRC. Proteomics revealed potential targets of these miRNAs involved in sensitivity to chemotherapy.

2019-09-27 | PXD015369 | Pride

Translational reprogramming of colorectal cancer cells induced by 5-fluorouracil through a miRNA-dependent mechanism

Project description:5-Fluorouracil (5-FU) is a widely used chemotherapeutic drug in colorectal cancer. Previous studies showed that 5-FU modulates RNA metabolism and mRNA expression. In addition, it has been reported that 5-FU incorporates into the RNAs constituting the translational machinery and that 5-FU affects the amount of some mRNAs associated with ribosomes. However, the impact of 5-FU on translational regulation remains unclear. Using translatome profiling, we report that a clinically relevant dose of 5-FU induces a translational reprogramming in colorectal cancer cell lines. Comparison of mRNA distribution between polysomal and non-polysomal fractions in response to 5-FU treatment using microarray quantification identified 313 genes whose translation was selectively regulated. These regulations were mostly stimulatory (91%). Among these genes, we showed that 5-FU increases the mRNA translation of HIVEP2, which encodes a transcription factor whose translation in normal condition is known to be inhibited by mir-155. In response to 5-FU, the expression of mir-155 decreases thus stimulating the translation of HIVEP2 mRNA. Interestingly, the 5-FU-induced increase in specific mRNA translation was associated with reduction of global protein synthesis. Altogether, these findings indicate that 5-FU promotes a translational reprogramming leading to the increased translation of a subset of mRNAs that involves at least for some of them, miRNA-dependent mechanisms. This study supports a still poorly evaluated role of translational control in drug response.

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Mouse Liver LC-MS/MS LNA miR-676 treated dbdb mice

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2017-11-14 | PXD006573 | Pride

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