hct116 vim rfp  (ATCC)

Journal: Journal of Translational Medicine

Article Title: FFAR4 negatively regulates colorectal cancer growth via blocking oxidative phosphorylation

doi: 10.1186/s12967-026-07942-4

Figure Lengend Snippet: FFAR4 activator TUG891 reduces cell growth. ( A - B ) CCK-8 assays showing the effects of increasing concentrations of TUG891 (0–80 µM) on the proliferation of HCT116 and HT29 cells after 48 h. ( C ) Flow cytometric analysis of cell cycle distribution in HCT116 (upper panel) and HT29 (lower panel) cells following treatment with increasing concentrations of TUG891. ( D ) Western blot analysis of Cyclin D1 expression in CRC cells treated with 40 µM TUG891 in HCT116 (upper panel) and HT29 (lower panel) cells. ( E ) Flow cytometric analysis of apoptosis in CRC cells following TUG891 treatment, as assessed by Annexin V/PI staining. ( F ) Validation of FFAR4 knockdown efficiency at both the mRNA and protein levels. ( G ) CCK-8 assays assessing cell proliferation in control, FFAR4 knockdown, TUG891-treated, and combined FFAR4 knockdown plus TUG891 groups. ( H ) Cell cycle analysis showing the effects of FFAR4 knockdown on TUG891-induced G0/G1 phase arrest. Data are presented as the mean ± standard deviation (SD). Statistical significance was determined using one-way ANOVA followed by Tukey’s multiple comparisons tests. Exact P values are shown for significant differences. ns, not significant ( P ≥ 0.05)

Article Snippet: Human colorectal cancer cell lines HCT116 (CCL-247EMT; ATCC) and HT29 (HTB-38; ATCC) were obtained from the Shanghai Institute of Cell Biology, Chinese Academy of Sciences, Shanghai, China.

Techniques: CCK-8 Assay, Western Blot, Expressing, Staining, Biomarker Discovery, Knockdown, Control, Cell Cycle Assay, Standard Deviation

Journal: Journal of Translational Medicine

Article Title: FFAR4 negatively regulates colorectal cancer growth via blocking oxidative phosphorylation

doi: 10.1186/s12967-026-07942-4

Figure Lengend Snippet: FFAR4 activation promotes glycolysis and is associated with inhibition of oxidative phosphorylation. ( A ) Medium color shift observed in HCT116 cultures treated with increasing concentrations of TUG891. ( B ) TUG891-induced modulation of lactate secretion in HCT116 medium at 40 µM concentration. ( C ) Color shift in HT29 culture medium following treatment with increasing TUG891 concentrations. ( D ) Modulation of medium lactate content in HT29 cells following treatment with 40 µM TUG891. ( E ) Evaluation of TUG891-mediated antitumor effects in HCT116 (upper) and HT29 (lower) cells under pH-stabilized conditions achieved through NaHCO₃ addition or regular medium renewal. ( F ) Lactate metabolic pathway. ( G ) Effects of glucose supplementation on TUG891’s antitumor activity in HCT116 (left) and HT29 (right) cells. ( H ) Effect of 40 µM TUG891 on extracellular acidification rate (ECAR) in HCT116 (left) and HT29 (right) cells. ( I ) Impact of 40 µM TUG891 on oxygen consumption rate (OCR) in HCT116 (left) and HT29 (right) cells. Data are presented as mean ± standard deviation (SD). Statistical significance was determined using one-way ANOVA and Tukey’s multiple comparisons tests. ns, not significant ( P ≥ 0.05)

Article Snippet: Human colorectal cancer cell lines HCT116 (CCL-247EMT; ATCC) and HT29 (HTB-38; ATCC) were obtained from the Shanghai Institute of Cell Biology, Chinese Academy of Sciences, Shanghai, China.

Techniques: Activation Assay, Inhibition, Phospho-proteomics, Concentration Assay, Activity Assay, Standard Deviation

Journal: Journal of Translational Medicine

Article Title: FFAR4 negatively regulates colorectal cancer growth via blocking oxidative phosphorylation

doi: 10.1186/s12967-026-07942-4

Figure Lengend Snippet: TUG891 reduces the NAD⁺/NADH ratio and disrupts mitochondrial redox homeostasis. ( A - B ) Principal-component analysis (PCA) of gene expression data, showing the clustering of gene profiles for control and FFAR4 activation groups in HCT116 cells ( A ) and HT29 cells ( B ). ( C ) Changes in metabolite levels with and without TUG891 treatment in HCT116 cells (upper panel) and HT29 cells (lower panel). Log2(FC) indicates log2-transformed fold change of the TUG891-treated group relative to the control group. ( D - E ) Over-Representation Analysis identified significantly enriched KEGG pathways based on different metabolites in HCT116 cells ( D ) and HT29 cells ( E ). ( F ) Western blot analysis of malate–aspartate shuttle–related enzymes (GOT1, GOT2, MDH1, and MDH2) and OXPHOS proteins in control and TUG891-treated cells. ( G - H ) Measurement of NAD + levels and the NAD + /NADH ratio in HCT116 cells comparing vehicle and FFAR4 activator groups. ( I - J ) Measurement of NAD + levels and the NAD + /NADH ratio in HT29 cells comparing vehicle and FFAR4 activator groups. ( K , L ) Measurement of the cellular ATP/ADP ratio in HCT116 ( K ) and HT29 ( L ) cells comparing vehicle and FFAR4 activator–treated groups. The data were expressed as the mean ± standard deviation (SD)

Article Snippet: Human colorectal cancer cell lines HCT116 (CCL-247EMT; ATCC) and HT29 (HTB-38; ATCC) were obtained from the Shanghai Institute of Cell Biology, Chinese Academy of Sciences, Shanghai, China.

Techniques: Gene Expression, Control, Activation Assay, Transformation Assay, Western Blot, Standard Deviation

Journal: bioRxiv

Article Title: MechanoMR microparticle (M 3 ) sensors reveal dynamic stress loading as a driver of epithelial-mesenchymal transition

doi: 10.64898/2025.12.10.693598

Figure Lengend Snippet: a, Schematic of 2D tumor spheroid arrays embedded with M 3 sensors via sacrificial micromolding. b, The sensor integration into the spheroid array was detected by correlated CFM and MR imaging. (bottom; green, alginate). Scale bar, 500 µm. c , Quantitative stress mapping over the 7-day spheroid growth using the M 3 sensor. Three cell lines (HCT116, A549, and MDA-MB-231) ( n = 10, 13, and 11, respectively) were used for comparision. d - g, Stress development during fibrosis of MRC5 spheroids. A schematic ( d ), CFM, and MR images of fibrotic spheroids with or without fibrosis inhibitor, nintedanib ( e ). Scale bar, 100 μm. Normalized T 2 * signals ( f ) and stress ( g ) of the fibrotic spheroids with or without nintedanib treatment ( n = 11 for (-) and n = 8 for (+)). h - k, Stress dynamics under epithelial-mesenchymal transition (EMT) of tumor spheroids. HCT116-vimentin-RFP reporter cells were used to detect EMT. A schematic ( h ), CFM, and MR images of HCT116 spheroids with or without EMT-inducer, 5-azacytidine ( i ). Scale bar, 100 μm. Normalized T 2 * signals ( j ) and stress ( k ) of HCT116 spheroids u with or without 5-azacytidine treatment ( n = 9 for (-) and n = 12 for (+)). Data are presented as mean ± s.d. Statistical significance was determined by one-way ANOVA with Tukey’s multiple comparisons test for ( c ), and by two-tailed unpaired Student’s t-test for ( g ) and ( k ). ****P < 0.0001; **P < 0.01; *P < 0.05.

Article Snippet: HCT116 vimRFP (CCL-247EMT, ATCC) cells were used to establish tumors for in vivo experiments.

Techniques: Imaging, Two Tailed Test

Journal: bioRxiv

Article Title: MechanoMR microparticle (M 3 ) sensors reveal dynamic stress loading as a driver of epithelial-mesenchymal transition

doi: 10.64898/2025.12.10.693598

Figure Lengend Snippet: a, Schematic of 2D tumor spheroid arrays embedded with M 3 sensors via sacrificial micromolding. b, The sensor integration into the spheroid array was detected by correlated CFM and MR imaging. (bottom; green, alginate). Scale bar, 500 µm. c , Quantitative stress mapping over the 7-day spheroid growth using the M 3 sensor. Three cell lines (HCT116, A549, and MDA-MB-231) ( n = 10, 13, and 11, respectively) were used for comparision. d - g, Stress development during fibrosis of MRC5 spheroids. A schematic ( d ), CFM, and MR images of fibrotic spheroids with or without fibrosis inhibitor, nintedanib ( e ). Scale bar, 100 μm. Normalized T 2 * signals ( f ) and stress ( g ) of the fibrotic spheroids with or without nintedanib treatment ( n = 11 for (-) and n = 8 for (+)). h - k, Stress dynamics under epithelial-mesenchymal transition (EMT) of tumor spheroids. HCT116-vimentin-RFP reporter cells were used to detect EMT. A schematic ( h ), CFM, and MR images of HCT116 spheroids with or without EMT-inducer, 5-azacytidine ( i ). Scale bar, 100 μm. Normalized T 2 * signals ( j ) and stress ( k ) of HCT116 spheroids u with or without 5-azacytidine treatment ( n = 9 for (-) and n = 12 for (+)). Data are presented as mean ± s.d. Statistical significance was determined by one-way ANOVA with Tukey’s multiple comparisons test for ( c ), and by two-tailed unpaired Student’s t-test for ( g ) and ( k ). ****P < 0.0001; **P < 0.01; *P < 0.05.

Article Snippet: HCT116 vimRFP cell line was purchased from ATCC (CCL-247EMT) and grown in McCoy’s medium (Gibco).

Techniques: Imaging, Two Tailed Test