Journal: Cell Death Discovery

Article Title: hnRNP A1 inhibits colorectal cancer tumorigenesis and progression by regulating fatty acid metabolism and RNA stability

doi: 10.1038/s41420-025-02814-0

Figure Lengend Snippet: A , B hnRNP A1 expression levels in six CRC cell lines and NCM460 determined by Western blotting, n = 3 per group. C hnRNP A1 expression levels in six CRC cell lines and NCM460 determined by qRT-PCR, n = 3 per group. D , E Western blotting verify the shRNA-mediated deletion of hnRNP A1 in RKO and Caco2 cells, n = 3 per group. F qRT-PCR verify the shRNA-mediated deletion of hnRNP A1 in RKO and Caco2 cells, n = 3 per group. G , H CCK-8 assay for assessing cell proliferation, n = 6 per group. I The proliferation ability of the cells was verified by clonal formation assay, n = 3 per group. J , K Transwell assay for assessing cell migration(Scale bar: 100 μm), n = 3 per group. L , M Wound-healing assay for assessing cell migration(Scale bar: 200 μm), n = 5 per group. ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Article Snippet: Human CRC cell lines RKO, Caco2, HT29, HCT116, SW480, and SW620 were purchased from Servicebio (Wuhan, China).

Techniques: Expressing, Western Blot, Quantitative RT-PCR, shRNA, CCK-8 Assay, Tube Formation Assay, Transwell Assay, Migration, Wound Healing Assay

Journal: Cell Death Discovery

Article Title: hnRNP A1 inhibits colorectal cancer tumorigenesis and progression by regulating fatty acid metabolism and RNA stability

doi: 10.1038/s41420-025-02814-0

Figure Lengend Snippet: A The mRNA with differential expression in RKO-nc and RKO-sh hnRNP A1 cells was analyzed by the KEGG pathway after RNA sequencing. B The KEGG pathway was analyzed after the hnRNP A1-binding protein was analyzed by RIP sequencing. C – F Western blotting demonstrates the expression changes of Bax and Bcl-2 in hnRNP A1-silenced cells, n = 3 per group. G , H The total apoptotic cells with the treatment of Adarotene for 24 h in RKO and Caco2 cells, n = 3 per group. I , J The number of genes shared after the intersection of RNA-seq and RIP-seq. K Fold change of 56 genes after screening. L Predicted hnRNP A1 and PPARα binding sites identified by RIP-seq. M A dual-luciferase reporter assay was used to assess the interaction between hnRNP A1 and the PPARα 3′UTR, n = 3 per group. N PPARα expression levels in CRC cell lines determined by qRT-PCR, n = 3 per group. O , P PPARα expression levels in CRC cell lines determined by Western blotting, n = 3 per group.* P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Article Snippet: Human CRC cell lines RKO, Caco2, HT29, HCT116, SW480, and SW620 were purchased from Servicebio (Wuhan, China).

Techniques: Quantitative Proteomics, RNA Sequencing, Binding Assay, Sequencing, Western Blot, Expressing, Luciferase, Reporter Assay, Quantitative RT-PCR

Journal: Cell Death Discovery

Article Title: hnRNP A1 inhibits colorectal cancer tumorigenesis and progression by regulating fatty acid metabolism and RNA stability

doi: 10.1038/s41420-025-02814-0

Figure Lengend Snippet: A The binding level of hnRNPA1 to PPARα in CRC cell lines was determined by RIP, n = 4 per group. B , C CCK-8 assay was used to determine cell proliferation after interference with PPARα gene, n = 6 per group. D The Transwell assay assesses the migration ability of cells after interference with the PPARα gene (Scale bar: 100 μm), n = 3 per group. E The number of apoptotic cells in RKO and Caco2 cells after PPARα gene interference was determined by flow cytometry, n = 3 per group. F , G The number of apoptotic cells in RKO and Caco2 cells after PPARα gene interference was determined by TUNEL (Scale bar: 50 μm), n = 6 per group. H The expression level of PPARα in cells treated with Act D at different time periods, n = 3 per group. I Cell activity after treatment with Act D, n = 6 per group. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Article Snippet: Human CRC cell lines RKO, Caco2, HT29, HCT116, SW480, and SW620 were purchased from Servicebio (Wuhan, China).

Techniques: Binding Assay, CCK-8 Assay, Transwell Assay, Migration, Flow Cytometry, TUNEL Assay, Expressing, Activity Assay

Journal: Cell Death Discovery

Article Title: hnRNP A1 inhibits colorectal cancer tumorigenesis and progression by regulating fatty acid metabolism and RNA stability

doi: 10.1038/s41420-025-02814-0

Figure Lengend Snippet: A , B Cell activity at different OA concentrations, n = 3 per group. C The expression level of PPARα after OA treatment. D , E Cell viability at various time points after OA treatment, n = 6 per group. F , G Neutral lipid content of RKO (hnRNP A1-nc/sh) and Caco2 (nc/sh) cells and cells after addition of OA (Scale bar: 50 μm), n = 3 per group. H , I Lipid droplet content of RKO (hnRNP A1-nc/sh) and Caco2 (nc/sh) cells and cells after addition of OA (Scale bar: 50 μm). J qRT-PCR demonstrates the effect of hnRNP A1 silencing on the expression of FASN, ACC1, ACLY, SCD1, CPT1A, CPT1B, ACOX1, and ACOX2 in CRC cells, n = 3 per group. K , L Western blotting reveals the expression changes of Bax and Bcl-2 expression in hnRNP A1-silenced cells treated with Act D. M , N Western blotting reveals the expression changes of PARP1, Cleaved-parp, Caspase3, Cleaved-caspase3, PPARα and hnRNP A1 expression in hnRNP A1-silenced cells treated with Act D. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Article Snippet: Human CRC cell lines RKO, Caco2, HT29, HCT116, SW480, and SW620 were purchased from Servicebio (Wuhan, China).

Techniques: Activity Assay, Expressing, Quantitative RT-PCR, Western Blot