Journal: Cellular Oncology (Dordrecht, Netherlands)

Article Title: METTL1-mediated m 7 G tRNA modification promotes colorectal cancer progression and liver metastasis via translational regulation

doi: 10.1007/s13402-025-01137-7

Figure Lengend Snippet: Knockout of METTL1 inhibits malignant capability of CRC cells. ( A ) Western blot verifying the efficiency of METTL1 knockout in DLD-1 and HCT116 CRC cell lines. ( B ) CCK-8 assay showing a decreased proliferative capacity of METTL1-knockout CRC cells compared with control cells. ( C ) Colony formation assay showing reduced clonogenic potential in METTL1-knockout CRC cells. ( D – E ) Migration ( D ) and Invasion ( E ) assays showing reduced migratory abilities and invasive abilities in METTL1-knockout CRC cells. β-actin was used for western blot loading control. *** P < 0.001, **** P < 0.0001. sgNC (single-guide RNA negative control), sgM1-1 (sgMETTL1-1) and sgM1-2 (sgMETTL1-2)

Article Snippet: The human colorectal cancer cell lines DLD-1 and HCT116 were obtained from the American Type Culture Collection (ATCC).

Techniques: Knock-Out, Western Blot, CCK-8 Assay, Control, Colony Assay, Migration, Negative Control

Journal: Cellular Oncology (Dordrecht, Netherlands)

Article Title: METTL1-mediated m 7 G tRNA modification promotes colorectal cancer progression and liver metastasis via translational regulation

doi: 10.1007/s13402-025-01137-7

Figure Lengend Snippet: Overexpression of METTL1 promotes malignant phenotypes of CRC cells. ( A ) Western blot confirming the overexpression efficiency of METTL1 in DLD-1 and HCT116 CRC cell lines. ( B ) CCK-8 assay showing increased proliferative capacity of CRC cells overexpressing wild-type METTL1 compared with control cells, while mutant METTL1 had little such effect. ( C ) Colony formation assay showing increased clonogenic potential in CRC cells overexpressing wild-type METTL1, while mutant METTL1 had little such effect. ( D – E ) Migration ( D ) and Invasion ( E ) assays showing increased migratory and invasive abilities of CRC cells overexpressing wild-type METTL1 compared with control cells, with representative images and quantification, while mutant METTL1 had little such effect. β-actin was used for western blot loading control. ** P < 0.01, **** P < 0.0001. oeNC (overexpression negative control, empty vector), oeWT (overexpression of wild-type METTL1) and oeMut (overexpression of catalytically inactive mutant METTL1)

Article Snippet: The human colorectal cancer cell lines DLD-1 and HCT116 were obtained from the American Type Culture Collection (ATCC).

Techniques: Over Expression, Western Blot, CCK-8 Assay, Control, Mutagenesis, Colony Assay, Migration, Negative Control, Plasmid Preparation

Journal: Cellular Oncology (Dordrecht, Netherlands)

Article Title: METTL1-mediated m 7 G tRNA modification promotes colorectal cancer progression and liver metastasis via translational regulation

doi: 10.1007/s13402-025-01137-7

Figure Lengend Snippet: METTL1 regulates tRNA m 7 G modification and translation efficiency in CRC cell lines. ( A ) Northwestern blot showing a marked reduction of tRNA m 7 G modification levels in METTL1-knockout CRC cells compared with control cells. ( B – C ) TRAC-seq identifying 16 m 7 G-modified tRNAs ( B ) and the “RGGUY” motif sequence at the tRNA m 7 G site ( C ) in the DLD-1 cell line. ( D – E ) Representative images ( D ) and quantification ( E ) showing decreased cleavage scores of m 7 G-modified tRNAs in METTL1-knockout DLD-1 cells. ( F ) Heatmap showing the expression profiles of m 7 G-modified tRNAs identified by TRAC-seq, indicating that METTL1 knockout leads to downregulation of most m 7 G-modified tRNAs. ( G ) Quantitative analysis of the relative expression changes of tRNAs in METTL1-knockout DLD-1 cells compared to control cells showing greater downregulation of m 7 G-modified tRNAs than unmodified tRNAs. Fold change was calculated as the ratio of tRNA expression level of METTL1-knockout group to the control group. ( H ) Polysome profiling showing reduced polyribosome peaks in METTL1-knockout DLD-1 cells. ( I–J ) Puromycin intake assay showing reduced translation efficiency in METTL1-depleted cells ( I ) and restoration in cells rescued with wild type METTL1, but not its catalytically inactive mutant ( J ). β-actin was used for western blot loading control. U6 snRNA was used for northwestern blot loading control. *** P < 0.001. siNC (small interfering RNA negative control), siM1-1 (siMETTL1-1) and siM1-2 (siMETTL1-2). oeNC (overexpression negative control, empty vector), oeWT (overexpression of wild-type METTL1) and oeMut (overexpression of catalytically inactive mutant METTL1)

Article Snippet: The human colorectal cancer cell lines DLD-1 and HCT116 were obtained from the American Type Culture Collection (ATCC).

Techniques: Modification, Knock-Out, Control, Sequencing, Expressing, Mutagenesis, Western Blot, Small Interfering RNA, Negative Control, Over Expression, Plasmid Preparation