Journal: Frontiers in Oncology

Article Title: Emodin inhibits colon cancer tumor growth by suppressing tumor cell glycolysis through inhibition of NAT10-mediated PGK1 ac4C modification

doi: 10.3389/fonc.2025.1575391

Figure Lengend Snippet: Emodin inhibited cell viability of colon cancer cells. (A) The molecular structure of emodin. (B, C) Cell viability of HCT-116 and SW480 cells was measured by MTT assay. N = 3 per group. Data analysis was performed using ANOVA.

Article Snippet: Extracellular acidification rate (ECAR) of HCT-116 and SW480 cells was measured using an ECAR fluorometric assay kit (Elabscience, Wuhan, China).

Techniques: MTT Assay

Journal: Frontiers in Oncology

Article Title: Emodin inhibits colon cancer tumor growth by suppressing tumor cell glycolysis through inhibition of NAT10-mediated PGK1 ac4C modification

doi: 10.3389/fonc.2025.1575391

Figure Lengend Snippet: Emodin inhibited cell proliferation and glycolysis in colon cancer cells. (A, B) Cell proliferation was evaluated by EdU staining. (C) Glucose uptake of HCT-116 and SW480 cells was measured using a glucose uptake assay kit. (D) Lactate production was evaluated using a lactate content detection kit. (E, F) Real-time cell metabolism was assessed by measuring ECAR. N = 3 per group. Data analysis was performed using ANOVA.

Article Snippet: Extracellular acidification rate (ECAR) of HCT-116 and SW480 cells was measured using an ECAR fluorometric assay kit (Elabscience, Wuhan, China).

Techniques: Staining

Journal: Frontiers in Oncology

Article Title: Emodin inhibits colon cancer tumor growth by suppressing tumor cell glycolysis through inhibition of NAT10-mediated PGK1 ac4C modification

doi: 10.3389/fonc.2025.1575391

Figure Lengend Snippet: Emodin suppressed ac4C modification by inhibiting NAT10 expression in colon cancer cells. (A, B) The ac4C levels of HCT-116 and SW480 cells were detected by dot blot assay. (C) The expression of NAT10 in HCT-116 and SW480 cells was measured by qPCR. (D) The protein levels of NAT10 in HCT-116 and SW480 cells were detected by western blot. The interaction between NAT10 and eomdin was determined by (E) molecular docking and (F) SRP assay. N = 3 per group. Data analysis was performed using student’s t-test.

Article Snippet: Extracellular acidification rate (ECAR) of HCT-116 and SW480 cells was measured using an ECAR fluorometric assay kit (Elabscience, Wuhan, China).

Techniques: Modification, Expressing, Dot Blot, Western Blot

Journal: Frontiers in Oncology

Article Title: Emodin inhibits colon cancer tumor growth by suppressing tumor cell glycolysis through inhibition of NAT10-mediated PGK1 ac4C modification

doi: 10.3389/fonc.2025.1575391

Figure Lengend Snippet: NAT10 overexpression restored glycolysis inhibited by emodin in colon cancer cells. (A) The expression of NAT10 was measured by qPCR. (B) The protein levels of NAT10 were detected by western blot. (C, D) Cell proliferation of HCT-116 and SW480 cells was evaluated by EdU staining. (E) Glucose uptake was evaluated using a glucose uptake assay kit. (F) Lactate production was evaluated using a lactate content detection kit. (G) Real-time cell metabolism was assessed by measuring ECAR. (H) The protein levels of HK2, PFK1 and LDHA were detected by western blot. N = 3 per group. Data analysis was performed using student’s t-test (A) or ANOVA (D–G) .

Article Snippet: Extracellular acidification rate (ECAR) of HCT-116 and SW480 cells was measured using an ECAR fluorometric assay kit (Elabscience, Wuhan, China).

Techniques: Over Expression, Expressing, Western Blot, Staining

Journal: Frontiers in Oncology

Article Title: Emodin inhibits colon cancer tumor growth by suppressing tumor cell glycolysis through inhibition of NAT10-mediated PGK1 ac4C modification

doi: 10.3389/fonc.2025.1575391

Figure Lengend Snippet: NAT10 knockdown suppressed PGK1 mRNA stability by inhibiting its ac4C modification. (A) The expression of NAT10 was measured by qPCR. (B) The protein levels of NAT10 were detected by western blot. (C) The expression of PGK1 was measured by qPCR. (D) The protein levels of PGK1 were detected by western blot. (E) The ac4C levels of HCT-116 and SW480 cells were detected by MeRIP. (F) The ac4C modification site of PGK1 was predicted using the PACES database. (G) The interaction between NAT10 and PGK1 was identified by RIP. (H) The luciferase activity of WT-PGK1 and MUT-PGK1 of HCT-116 cells. (I) The stability of PGK1 mRNA was measured by qPCR after HCT-116 cells treated with 5 μg/mL actinomycin D for 0, 4, 8, and 12 h. N = 3 per group. Data analysis was performed using student’s t-test (A, C, D, G) or ANOVA (F, H) .

Article Snippet: Extracellular acidification rate (ECAR) of HCT-116 and SW480 cells was measured using an ECAR fluorometric assay kit (Elabscience, Wuhan, China).

Techniques: Knockdown, Modification, Expressing, Western Blot, Luciferase, Activity Assay

Journal: Frontiers in Oncology

Article Title: Emodin inhibits colon cancer tumor growth by suppressing tumor cell glycolysis through inhibition of NAT10-mediated PGK1 ac4C modification

doi: 10.3389/fonc.2025.1575391

Figure Lengend Snippet: Cell proliferation and glycolysis of colon cancer cells inhibited by NAT10 knockdown was restored by PGK1 overexpression. (A) The expression of PGK1 was measured by qPCR. (B) The protein levels of PGK1 were detected by western blot. (C, D) Cell proliferation of HCT-116 and SW480 cells was evaluated by EdU staining. (E) Glucose uptake was evaluated using a glucose uptake assay kit. (F) Lactate production was evaluated using a lactate content detection kit. (G) Real-time cell metabolism was assessed by measuring ECAR. (H) The protein levels of HK2, PFK1 and LDHA were detected by western blot. N = 3 per group. Data analysis was performed using student’s t-test (A) or ANOVA (D–G) .

Article Snippet: Extracellular acidification rate (ECAR) of HCT-116 and SW480 cells was measured using an ECAR fluorometric assay kit (Elabscience, Wuhan, China).

Techniques: Knockdown, Over Expression, Expressing, Western Blot, Staining