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| Status |
Public on May 20, 2024 |
| Title |
Small RNAseq using tumor-derived extracellular vesicles |
| Organism |
Homo sapiens |
| Experiment type |
Non-coding RNA profiling by high throughput sequencing
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| Summary |
RNA modifications play important roles in cellular processes, and their dysregulation has been linked to various diseases, including cancer. As extracellular vesicles (EVs) contain various RNAs, it is assumed that these can be modified. However, the presence of such modified transcripts has not been determined due to the small amount of RNAs in EVs. Herein, we successfully detected 22 RNA modifications in EVs using a proprietary ultra-high performance liquid chromatography tandem mass spectrometry system and identified reduced levels of N6-methyladenosine (m6A) in EVs derived from colon cancer tissues, which correlated with cancer recurrence. Increasing m6A modification levels in colorectal cancer EVs via m6A demethylase Alkbh5 knockout suppressed the tumor-promoting effect of colorectal cancer EVs. Mechanistically, colorectal cancer-derived EVs increased tumor necrotic factor a and interleukin-6 secretion by macrophages via toll-like receptor 8 in an m6A-dependent manner and promoted cancer cell proliferation. RNA-seq analysis showed that 5’-tRF-GlyGCC were enriched in colorectal cancer EVs, and m6A levels on 5’-tRF-GlyGCC were decreased in colorectal cancer EVs compared with those in normal colon EVs. Cancer-derived EVs containing 5’-tRF-GlyGCC significantly promoted tumor growth, and the effect was impeded through macrophage depletion. These data provide evidence that cancer-specific RNA modifications are present in EVs, promoting tumor progression by regulating immune cells.
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| Overall design |
To investigate the colon cancer-charachteristic small RNA in EVs, we analyzed EV-RNA from colon cancer-tissue derived EVs (small EVs=6, large EVs=6) and adjacent norrmal colon-tissue derived EVs (small EVs=6, large EVs=6).
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| Contributor(s) |
Jingushi K, Monoe Y, Takano Y, Hirosuna K, Taniguchi K, Komura K, Lee S, Tsujikawa K |
| Citation missing |
Has this study been published? Please login to update or notify GEO. |
| Submission date |
May 20, 2024 |
| Last update date |
May 21, 2024 |
| Contact name |
Kentaro Jingushi |
| E-mail(s) |
jingushi-kk@phs.osaka-u.ac.jp
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| Phone |
+81-6-6879-8192
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| Organization name |
Osaka University
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| Department |
Graduate School of Pharmaceutical Sciences
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| Lab |
Laboratory of Molecular and Cellular Physiology
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| Street address |
1-6 Yamadaoka
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| City |
Suita |
| State/province |
Osaka |
| ZIP/Postal code |
565-0871 |
| Country |
Japan |
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| Platforms (1) |
| GPL16791 |
Illumina HiSeq 2500 (Homo sapiens) |
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| Samples (24)
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| GSM8282451 |
Colon cancer EVs, 37T, LEVs |
| GSM8282452 |
Colon cancer EVs, 39T, LEVs |
| GSM8282453 |
Colon cancer EVs, 40T, LEVs |
| GSM8282454 |
Adjacent normal colon tissue EVs, 30N, LEVs |
| GSM8282455 |
Adjacent normal colon tissue EVs, 34N, LEVs |
| GSM8282456 |
Adjacent normal colon tissue EVs, 35N, LEVs |
| GSM8282457 |
Adjacent normal colon tissue EVs, 37N, LEVs |
| GSM8282458 |
Adjacent normal colon tissue EVs, 39N, LEVs |
| GSM8282459 |
Adjacent normal colon tissue EVs, 40N, LEVs |
| GSM8282460 |
Colon cancer EVs, 30T, sEVs |
| GSM8282461 |
Colon cancer EVs, 34T, sEVs |
| GSM8282462 |
Colon cancer EVs, 35T, sEVs |
| GSM8282463 |
Colon cancer EVs, 37T, sEVs |
| GSM8282464 |
Colon cancer EVs, 39T, sEVs |
| GSM8282465 |
Colon cancer EVs, 40T, sEVs |
| GSM8282466 |
Adjacent normal colon tissue EVs, 30N, sEVs |
| GSM8282467 |
Adjacent normal colon tissue EVs, 34N, sEVs |
| GSM8282468 |
Adjacent normal colon tissue EVs, 35N, sEVs |
| GSM8282469 |
Adjacent normal colon tissue EVs, 37N, sEVs |
| GSM8282470 |
Adjacent normal colon tissue EVs, 39N, sEVs |
| GSM8282471 |
Adjacent normal colon tissue EVs, 40N, sEVs |
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| Relations |
| BioProject |
PRJNA1113693 |
| Supplementary file |
Size |
Download |
File type/resource |
| GSE267953_RAW.tar |
6.6 Mb |
(http)(custom) |
TAR (of TXT) |
SRA Run Selector |
| Raw data are available in SRA |
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