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Supplementary Fig. 1. Prognostic and Diagnostic Significance of MCM3 Expression in HCC. (A) MCM3 expression in tumor and adjacent normal tissues across multiple cancer types. (B) ROC curve illustrating MCM3’s diagnostic accuracy for liver cancer. (C) Kaplan-Meier survival analysis of progression-free interval (PFI) in TCGA cohort based on MCM3 expression. (D) Kaplan-Meier survival analysis of overall survival (OS) in ICGC cohort based on MCM3 expression. (E) Risk score plot based on MCM3 expression and overall survival (OS) in TCGA cohort. (F) Risk score plot based on MCM3 expression and overall survival (OS) in ICGC cohort.
Supplementary Fig. 2. MCM3 Regulates EMT, Cell Cycle, and Metastasis in HCC via AKT/Twist Signaling. (A) Representative protein expression of MCM3 in 12 matched HCC and paratumor tissues. (B) Percentage of lung metastases in patients with different levels of MCM3 expression. (C) The changes in the cell cycle of LM3 after MCM3 KD evaluated by flow cytometry. (D) The changes in the cell cycle of HepG2 after MCM3 OE evaluated by flow cytometry. (E) Twist protein expression in LM3 after KD. (F) Twist protein expression in HepG2 after OE. (G) Effect of AKT activator (SC-79) and AKT inhibitor (MK-2206) on the expression of EMT markers after MCM3 KD. (H) Effect of AKT activator (SC-79) and AKT inhibitor (MK-2206) on the expression of EMT markers after MCM3 OE. (I) The effect of MCM3 KD or OE on EMT process evaluated via IHC. Data are presented as mean ± SEM; *P < 0.05, **P < 0.01.
Supplementary Fig. 3. MCM3 Influences HCC Proliferation and Invasion via AKT Signaling Modulation. (A) The proliferation of LM3 after MCM3 KD and treatment with the AKT inhibitor MK-2206 evaluated by CCK-8 assays. (B) Invasion of LM3 after MCM3 KD and treatment with the AKT inhibitor MK-2206 evaluated by transwell assays. (C) The proliferation of HepG2 after MCM3 OE and treatment with the AKT activator SC-79 evaluated by CCK-8 assays. (D) Invasion of HepG2 after MCM3 OE and treatment with the AKT activator SC-79 evaluated by transwell assays. Data are presented as mean ± SEM; *P < 0.05, **P < 0.01.
Supplementary Fig. 1. Prognostic and Diagnostic Significance of MCM3 Expression in HCC. (A) MCM3 expression in tumor and adjacent normal tissues across multiple cancer types. (B) ROC curve illustrating MCM3’s diagnostic accuracy for liver cancer. (C) Kaplan-Meier survival analysis of progression-free interval (PFI) in TCGA cohort based on MCM3 expression. (D) Kaplan-Meier survival analysis of overall survival (OS) in ICGC cohort based on MCM3 expression. (E) Risk score plot based on MCM3 expression and overall survival (OS) in TCGA cohort. (F) Risk score plot based on MCM3 expression and overall survival (OS) in ICGC cohort.
Supplementary Fig. 2. MCM3 Regulates EMT, Cell Cycle, and Metastasis in HCC via AKT/Twist Signaling. (A) Representative protein expression of MCM3 in 12 matched HCC and paratumor tissues. (B) Percentage of lung metastases in patients with different levels of MCM3 expression. (C) The changes in the cell cycle of LM3 after MCM3 KD evaluated by flow cytometry. (D) The changes in the cell cycle of HepG2 after MCM3 OE evaluated by flow cytometry. (E) Twist protein expression in LM3 after KD. (F) Twist protein expression in HepG2 after OE. (G) Effect of AKT activator (SC-79) and AKT inhibitor (MK-2206) on the expression of EMT markers after MCM3 KD. (H) Effect of AKT activator (SC-79) and AKT inhibitor (MK-2206) on the expression of EMT markers after MCM3 OE. (I) The effect of MCM3 KD or OE on EMT process evaluated via IHC. Data are presented as mean ± SEM; *P < 0.05, **P < 0.01.
Supplementary Fig. 3. MCM3 Influences HCC Proliferation and Invasion via AKT Signaling Modulation. (A) The proliferation of LM3 after MCM3 KD and treatment with the AKT inhibitor MK-2206 evaluated by CCK-8 assays. (B) Invasion of LM3 after MCM3 KD and treatment with the AKT inhibitor MK-2206 evaluated by transwell assays. (C) The proliferation of HepG2 after MCM3 OE and treatment with the AKT activator SC-79 evaluated by CCK-8 assays. (D) Invasion of HepG2 after MCM3 OE and treatment with the AKT activator SC-79 evaluated by transwell assays. Data are presented as mean ± SEM; *P < 0.05, **P < 0.01.