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Published on: November 26, 2010
tRF/miR-1280 Suppresses Stem Cell-like Cells and Metastasis in Colorectal Cancer
Bingqing Huang1,2, Huipeng Yang1, Xixi Cheng1
1Department of Immunology, Research Center of Basic Medical Sciences, Key Laboratory of Immune Microenvironment and Diseases of Educational Ministry of China, Tianjin Medical University, Tianjin, China.
Abstract:
Several studies have shown that tRNAs can be enzymatically cleaved to generate distinct classes of tRNA-derived fragments (tRF). Here, we report that tRF/miR-1280, a 17-bp fragment derived from tRNALeu and pre-miRNA, influences Notch signaling pathways that support the function of cancer stem-like cells (CSC) in colorectal cancer progression. tRF/miR-1280 expression was decreased in human specimens of colorectal cancer. Ectopic expression of tRF/miR-1280 reduced cell proliferation and colony formation, whereas its suppression reversed these effects. Mechanistic investigations implicated the Notch ligand JAG2 as a direct target of tRF/miR-1280 binding through which it reduced tumor formation and metastasis. Notably, tRF/miR-1280-mediated inactivation of Notch signaling suppressed CSC phenotypes, including by direct transcriptional repression of the Gata1/3 and miR-200b genes. These results were consistent with findings of decreased levels of miR-200b and elevated levels of JAG2, Gata1, Gata3, Zeb1, and Suz12 in colorectal cancer tissue specimens. Taken together, our results established that tRF/miR-1280 suppresses colorectal cancer growth and metastasis by repressing Notch signaling pathways that support CSC phenotypes. Furthermore, they provide evidence that functionally active miRNA can be derived from tRNA, offering potential biomarker and therapeutic uses. Cancer Res; 77(12); 3194-206. ©2017 AACR.
Insights
A novel tRNA-derived fragment, tRF/miR-1280, suppresses colorectal cancer growth by inhibiting Notch signaling pathways essential for cancer stem-like cells (CSC). This discovery offers potential new biomarkers and therapies for colorectal cancer.
Area of Science:
- Molecular Biology
- Cancer Research
- Epigenetics
Background:
- Transfer RNAs (tRNAs) can be cleaved into tRNA-derived fragments (tRFs).
- tRFs are implicated in various biological processes, including cancer progression.
- Notch signaling pathways are crucial for maintaining cancer stem-like cell (CSC) function.
Purpose of the Study:
- To investigate the role of tRF/miR-1280 in colorectal cancer (CRC) progression.
- To elucidate the molecular mechanisms by which tRF/miR-1280 affects CSCs and Notch signaling.
- To assess the potential of tRF/miR-1280 as a biomarker or therapeutic target in CRC.
Main Methods:
- Analysis of tRF/miR-1280 expression in human CRC specimens.
- Overexpression and suppression experiments to evaluate the functional impact of tRF/miR-1280 on CRC cells.
- Mechanistic studies to identify direct targets of tRF/miR-1280, including gene expression analysis and pathway investigation.
Main Results:
- tRF/miR-1280 expression was significantly decreased in human CRC tissues.
- Ectopic expression of tRF/miR-1280 inhibited CRC cell proliferation and colony formation.
- tRF/miR-1280 directly targets JAG2, inactivating Notch signaling and suppressing CSC phenotypes by repressing Gata1/3 and miR-200b.
Conclusions:
- tRF/miR-1280 acts as a tumor suppressor in colorectal cancer by inhibiting Notch signaling and CSC phenotypes.
- The findings highlight the functional role of tRNA-derived microRNAs (miRNAs) in cancer.
- tRF/miR-1280 presents a promising candidate for CRC biomarker and therapeutic strategies.
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