Chimeric RNA RRM2-C2orf48 plays an oncogenic role in the development of NNK-induced lung cancer
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ABSTRACT:
PROVIDER: PRJNA901865 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22297988_1.fastq.gz | Fastqsanger.gz | |||
| SRR22297988_2.fastq.gz | Fastqsanger.gz | |||
| SRR22297989_1.fastq.gz | Fastqsanger.gz | |||
| SRR22297989_2.fastq.gz | Fastqsanger.gz | |||
| SRR22297990_1.fastq.gz | Fastqsanger.gz |
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Project description:Chimeric RNAs have been used as biomarkers and therapeutic targets for multiple types of cancers. However, less attention has been paid to their mechanism of action in neoplasia. Here, we report that chimeric RNA RRM2-C2orf48 promotes 4-(methyl nitrosamine)-1-(3-pyridinyl)-1-butanone (NNK)-induced lung cancer. We found that RRM2-C2orf48 had higher expression levels in lung cancer cell lines and in lung cancer tissues from 74 patients than in normal cells and tissues, respectively. And its expression level was correlated with smoking. Next, we demonstrate that the expression level of RRM2-C2orf48 could increase after treatment with 200 mg/L NNK for 24 h. Overexpressing RRM2-C2orf48 accelerated the process of NNK-induced lung cancer and promoted cell growth. Meanwhile, suppressing RRM2-C2orf48 inhibited cell growth. Finally, we identified miR-219a-2-3p as a potential target of RRM2-C2orf48. In summary, RRM2-C2orf48 accelerated the process of NNK-induced lung cancer and miR-219a-2-3p may be involved in this process.
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Project description:Chimeric RNAs have been used as biomarkers and therapeutic targets for multiple types of cancers. However, less attention has been paid to their mechanism of action in neoplasia. Here, we reported that high-expressed chimeric RNA RRM2-C2orf48 was found in malignantly transformed BEAS-2B cells induced by 4-(methyl nitrosamine)-1-(3-pyridinyl)-1-butanone (NNK) in 74 lung cancer patients and several lung cancer cell lines. The expression level of RRM2-C2orf48 was significantly correlated with lymph node metastasis, distant metastasis, tumor-lymph node-metastasis (TNM) stage, and smoking. Overexpressing RRM2-C2orf48 promoted cell growth and accelerated the process of NNK-induced lung cancer. RRM2-C2orf48 knockdown inhibited the growth of RRM2-C2orf48-overexpressing BEAS-2B cells. Finally, we identified miR-219a-2-3p as a potential target of RRM2-C2orf48 in lung cancer. In summary, chimeric RNA RRM2-C2orf48 accelerated the process of NNK-induced lung cancer, and miR-219a-2-3p may be involved in this process.
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Project description:A microarray analysis was performed on the vector and over-expressing RRM2-c2orf48 NPC cell samples(CNE2-PMSCV-Vector and CNE2-PMSCV-RRM2-c2orf48). Total RNA was extracted from 1 × 106 cells using TRIzol reagent and was further purified using a Qiagen RNeasy Mini Kit according to the manufactures’ instructions. RNA quality was assessed by formaldehyde agarose gel electrophoresis and was quantitated spectrophotometrically. Total RNA was labeled and hybridized to the CapitalBio Corporation’s Affymetrix GeneChip Human Genome U133 Plus 2.0 Array (Affymetrix). We applied a two class unpaired method available through the Significant Analysis of Microarray software (SAM) to identify significantly differentially expressed genes between vector and over-expression samples. Genes were deemed significantly differentially expressed based on a selection threshold of a false discovery rate of FDR<5% and a fold change level of ＞1.5 in the SAM output results.
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Project description:TET1, the founding member of the TET family of enzymes (TET1/2/3) that convert 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC), was first identified as a partner gene in MLL-rearranged leukemia, but its definitive pathological role in leukemia is unclear. The down-regulation of all three TET genes and loss-of-function mutations of TET2 have been frequently observed in various cancers, and it was thought that they all play tumor-suppressor roles in tumorigenesis. Here we show that TET1 is likely a direct target of MLL and significantly up-regulated in MLL-rearranged leukemia, associated with an increased level of 5hmC. Our further in vitro and in vivo studies demonstrate that Tet1 plays an indispensable oncogenic role in MLL-rearranged leukemia, through cooperating with MLL fusion proteins in regulating their co-targets including the Hoxa/Meis1/Pbx3/Flt3 genes. Our data delineate a MLL-fusion/Tet1/Hoxa/Meis1/Pbx3/Flt3 signaling axis in MLL-rearranged leukemia, and highlight TET1 as a potential therapeutic target in treating this presently therapy-resistant disease.
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