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TRIM37 expression is upregulated in HCC tissues and cell lines, and its upregulation is linked to poor patient survival. (A) TRIM37 mRNA expression levels were assessed using TCGA dataset via online bioinformatics tools. (B) GEPIA2 analysis showed that TRIM37 overexpression relates to reduced overall survival in HCC patients. (C) qRT-PCR analysis of TRIM37 level in six paired HCC (T) and adjacent non-cancerous tissues (N). (D) Representative IHC images showing TRIM37 level in HCC tissues (T) and corresponding neighboring non-cancerous tissues (N) (magnification ×200). (E) Quantification of TRIM37 IHC staining scores in paired HCC (T) and neighboring healthy tissues (N). (F) WB analysis of TRIM37 protein level in HCC cell lines (HCCLM3, Huh7, HepG2, and Hep3B) compared to healthy liver epithelial cells (LO2). Each experiment was repeated at least three independent biological replicates. Data are reported as mean ± SD (n=3). *, P<0.05; **, P<0.01; ***, P<0.001. HCC, hepatocellular carcinoma; HR, hazard ratio; IHC, immunohistochemistry; LIHC, liver hepatocellular carcinoma; mRNA, messenger RNA; N, normal; qRT-PCR, quantitative real‑time polymerase chain reaction; SD, standard deviation; T, tumor; TCGA, The Cancer Genome Atlas; TPM, transcripts per million; WB, Western blot.

Journal: Translational Cancer Research

Article Title: TRIM37 interacts with PTEN to promote progression of hepatocellular carcinoma cells by modulating AKT/GSK-3β/β-Catenin pathway

doi: 10.21037/tcr-2026-0447

Figure Lengend Snippet: TRIM37 expression is upregulated in HCC tissues and cell lines, and its upregulation is linked to poor patient survival. (A) TRIM37 mRNA expression levels were assessed using TCGA dataset via online bioinformatics tools. (B) GEPIA2 analysis showed that TRIM37 overexpression relates to reduced overall survival in HCC patients. (C) qRT-PCR analysis of TRIM37 level in six paired HCC (T) and adjacent non-cancerous tissues (N). (D) Representative IHC images showing TRIM37 level in HCC tissues (T) and corresponding neighboring non-cancerous tissues (N) (magnification ×200). (E) Quantification of TRIM37 IHC staining scores in paired HCC (T) and neighboring healthy tissues (N). (F) WB analysis of TRIM37 protein level in HCC cell lines (HCCLM3, Huh7, HepG2, and Hep3B) compared to healthy liver epithelial cells (LO2). Each experiment was repeated at least three independent biological replicates. Data are reported as mean ± SD (n=3). *, P<0.05; **, P<0.01; ***, P<0.001. HCC, hepatocellular carcinoma; HR, hazard ratio; IHC, immunohistochemistry; LIHC, liver hepatocellular carcinoma; mRNA, messenger RNA; N, normal; qRT-PCR, quantitative real‑time polymerase chain reaction; SD, standard deviation; T, tumor; TCGA, The Cancer Genome Atlas; TPM, transcripts per million; WB, Western blot.

Article Snippet: The tissue portions were subsequently treated with a primary antibody targeting TRIM37 (DF14825, Affinity Biosciences, 1:60) overnight at 4 °C after being blocked with 5% BSA for 30 min. Assays for TRIM37 detection were conducted with the use of 3,3'-diaminobenzidine (DAB) chromogen and secondary antibodies coupled with horseradish peroxidase (HRP).

Techniques: Expressing, Over Expression, Quantitative RT-PCR, Immunohistochemistry, Polymerase Chain Reaction, Standard Deviation, Western Blot

TRIM37 enhances the proliferative potential of HCC cells. (A,B) WB was conducted to evaluate TRIM37 protein expression in cells transfected with TRIM37-specific shRNA or TRIM37 upregulation vectors. (C-E) The proliferative capacity of HCCLM3 and Huh7 cells was estimated using CCK-8 and colony formation assessments. HCCLM3 cell transfection was conducted with TRIM37 shRNA, and Huh7 cells with TRIM37 overexpression vectors (crystal violet stained). Each experiment was repeated at least three independent biological replicates. Data are reported as mean ± SD (n=3). *, P<0.05; **, P<0.01; ***, P<0.001. CCK-8, Cell Counting Kit-8; HCC, hepatocellular carcinoma; OD, optical density; SD, standard deviation; shRNA, short hairpin RNA; WB, Western blot.

Journal: Translational Cancer Research

Article Title: TRIM37 interacts with PTEN to promote progression of hepatocellular carcinoma cells by modulating AKT/GSK-3β/β-Catenin pathway

doi: 10.21037/tcr-2026-0447

Figure Lengend Snippet: TRIM37 enhances the proliferative potential of HCC cells. (A,B) WB was conducted to evaluate TRIM37 protein expression in cells transfected with TRIM37-specific shRNA or TRIM37 upregulation vectors. (C-E) The proliferative capacity of HCCLM3 and Huh7 cells was estimated using CCK-8 and colony formation assessments. HCCLM3 cell transfection was conducted with TRIM37 shRNA, and Huh7 cells with TRIM37 overexpression vectors (crystal violet stained). Each experiment was repeated at least three independent biological replicates. Data are reported as mean ± SD (n=3). *, P<0.05; **, P<0.01; ***, P<0.001. CCK-8, Cell Counting Kit-8; HCC, hepatocellular carcinoma; OD, optical density; SD, standard deviation; shRNA, short hairpin RNA; WB, Western blot.

Article Snippet: The tissue portions were subsequently treated with a primary antibody targeting TRIM37 (DF14825, Affinity Biosciences, 1:60) overnight at 4 °C after being blocked with 5% BSA for 30 min. Assays for TRIM37 detection were conducted with the use of 3,3'-diaminobenzidine (DAB) chromogen and secondary antibodies coupled with horseradish peroxidase (HRP).

Techniques: Expressing, Transfection, shRNA, CCK-8 Assay, Over Expression, Staining, Cell Counting, Standard Deviation, Western Blot

TRIM37 promotes invasion and EMT in HCC cells. (A,B) Transwell invasion assessments were conducted to evaluate the invasive capabilities of HCCLM3 and Huh7 cells transfected with TRIM37-specific shRNA or overexpression vectors (magnification ×200; crystal violet stained). (C,D) WB was used to examine the expression of EMT markers’ expression in each transfected group. Each experiment was repeated at least three independent biological replicates. Data are reported as mean ± SD (n=3). *, P<0.05; **, P<0.01; ***, P<0.001. EMT, epithelial-mesenchymal transition; HCC, hepatocellular carcinoma; SD, standard deviation; shRNA, short hairpin RNA; WB, Western blot.

Journal: Translational Cancer Research

Article Title: TRIM37 interacts with PTEN to promote progression of hepatocellular carcinoma cells by modulating AKT/GSK-3β/β-Catenin pathway

doi: 10.21037/tcr-2026-0447

Figure Lengend Snippet: TRIM37 promotes invasion and EMT in HCC cells. (A,B) Transwell invasion assessments were conducted to evaluate the invasive capabilities of HCCLM3 and Huh7 cells transfected with TRIM37-specific shRNA or overexpression vectors (magnification ×200; crystal violet stained). (C,D) WB was used to examine the expression of EMT markers’ expression in each transfected group. Each experiment was repeated at least three independent biological replicates. Data are reported as mean ± SD (n=3). *, P<0.05; **, P<0.01; ***, P<0.001. EMT, epithelial-mesenchymal transition; HCC, hepatocellular carcinoma; SD, standard deviation; shRNA, short hairpin RNA; WB, Western blot.

Article Snippet: The tissue portions were subsequently treated with a primary antibody targeting TRIM37 (DF14825, Affinity Biosciences, 1:60) overnight at 4 °C after being blocked with 5% BSA for 30 min. Assays for TRIM37 detection were conducted with the use of 3,3'-diaminobenzidine (DAB) chromogen and secondary antibodies coupled with horseradish peroxidase (HRP).

Techniques: Transfection, shRNA, Over Expression, Staining, Expressing, Standard Deviation, Western Blot

The PI3/AKT inhibitor LY294002 impairs TRIM37-mediated functions in Huh7 cells. (A,B) WB analysis of p-AKT, AKT, β-Catenin, p-GSK-3β, and GSK-3β expression in HCCLM3 and Huh7 cells transfected with TRIM37-specific shRNA or overexpression vectors. (C) WB analysis of the same proteins in TRIM37-overexpressing Huh7 cells exposed to LY294002. (D) CCK-8, (E) colony formation (crystal violet stained), and (F) Transwell invasion assessments were utilized to estimate the functional effects of LY294002 treatment on TRIM37-overexpressing Huh7 cells (magnification ×200, crystal violet stained). Each experiment was repeated at least three independent biological replicates. Data are reported as mean ± SD (n=3). *, P<0.05; **, P<0.01; ***, P<0.001. CCK-8, Cell Counting Kit-8; SD, standard deviation; shRNA, short hairpin RNA; WB, Western blot.

Journal: Translational Cancer Research

Article Title: TRIM37 interacts with PTEN to promote progression of hepatocellular carcinoma cells by modulating AKT/GSK-3β/β-Catenin pathway

doi: 10.21037/tcr-2026-0447

Figure Lengend Snippet: The PI3/AKT inhibitor LY294002 impairs TRIM37-mediated functions in Huh7 cells. (A,B) WB analysis of p-AKT, AKT, β-Catenin, p-GSK-3β, and GSK-3β expression in HCCLM3 and Huh7 cells transfected with TRIM37-specific shRNA or overexpression vectors. (C) WB analysis of the same proteins in TRIM37-overexpressing Huh7 cells exposed to LY294002. (D) CCK-8, (E) colony formation (crystal violet stained), and (F) Transwell invasion assessments were utilized to estimate the functional effects of LY294002 treatment on TRIM37-overexpressing Huh7 cells (magnification ×200, crystal violet stained). Each experiment was repeated at least three independent biological replicates. Data are reported as mean ± SD (n=3). *, P<0.05; **, P<0.01; ***, P<0.001. CCK-8, Cell Counting Kit-8; SD, standard deviation; shRNA, short hairpin RNA; WB, Western blot.

Article Snippet: The tissue portions were subsequently treated with a primary antibody targeting TRIM37 (DF14825, Affinity Biosciences, 1:60) overnight at 4 °C after being blocked with 5% BSA for 30 min. Assays for TRIM37 detection were conducted with the use of 3,3'-diaminobenzidine (DAB) chromogen and secondary antibodies coupled with horseradish peroxidase (HRP).

Techniques: Expressing, Transfection, shRNA, Over Expression, CCK-8 Assay, Staining, Functional Assay, Cell Counting, Standard Deviation, Western Blot

TRIM37 interacts with PTEN and promotes its ubiquitination. (A,B) WB analysis of PTEN protein level in HCCLM3 and Huh7 cells with TRIM37-specific shRNA or overexpression vectors. (C) qRT-PCR analysis of PTEN mRNA levels in HCCLM3 cells with TRIM37-specific shRNA. (D) Co-IP assays were conducted to evaluate the TRIM37 and PTEN interaction. (E) Ubiquitination assays were used to detect polyubiquitinated PTEN in HCCLM3 cells transfected with TRIM37-specific shRNA. Each experiment was repeated at least three independent biological replicates. Data are reported as mean ± SD (n=3). ns, not significant; *, P<0.05; **, P<0.01. Co-IP, co-immunoprecipitation; mRNA, messenger RNA; qRT-PCR, quantitative real‑time polymerase chain reaction; SD, standard deviation; shRNA, short hairpin RNA; WB, Western blot.

Journal: Translational Cancer Research

Article Title: TRIM37 interacts with PTEN to promote progression of hepatocellular carcinoma cells by modulating AKT/GSK-3β/β-Catenin pathway

doi: 10.21037/tcr-2026-0447

Figure Lengend Snippet: TRIM37 interacts with PTEN and promotes its ubiquitination. (A,B) WB analysis of PTEN protein level in HCCLM3 and Huh7 cells with TRIM37-specific shRNA or overexpression vectors. (C) qRT-PCR analysis of PTEN mRNA levels in HCCLM3 cells with TRIM37-specific shRNA. (D) Co-IP assays were conducted to evaluate the TRIM37 and PTEN interaction. (E) Ubiquitination assays were used to detect polyubiquitinated PTEN in HCCLM3 cells transfected with TRIM37-specific shRNA. Each experiment was repeated at least three independent biological replicates. Data are reported as mean ± SD (n=3). ns, not significant; *, P<0.05; **, P<0.01. Co-IP, co-immunoprecipitation; mRNA, messenger RNA; qRT-PCR, quantitative real‑time polymerase chain reaction; SD, standard deviation; shRNA, short hairpin RNA; WB, Western blot.

Article Snippet: The tissue portions were subsequently treated with a primary antibody targeting TRIM37 (DF14825, Affinity Biosciences, 1:60) overnight at 4 °C after being blocked with 5% BSA for 30 min. Assays for TRIM37 detection were conducted with the use of 3,3'-diaminobenzidine (DAB) chromogen and secondary antibodies coupled with horseradish peroxidase (HRP).

Techniques: Ubiquitin Proteomics, shRNA, Over Expression, Quantitative RT-PCR, Co-Immunoprecipitation Assay, Transfection, Immunoprecipitation, Polymerase Chain Reaction, Standard Deviation, Western Blot

TRIM37 facilitates HCC progression by inhibiting PTEN expression. (A) CCK-8 assessment was conducted to estimate the TRIM37-overexpressing Huh7 cell growth with or without PTEN upregulation. (B) Colony formation (crystal violet stained), and (C) Transwell invasion assessments were carried out to estimate the proliferative and invasive capabilities of TRIM37-upregulating Huh7 cells with or without PTEN upregulation (magnification ×200, crystal violet stained). (D) WB analysis of p-AKT, AKT, β-Catenin, p-GSK-3β, and GSK-3β expression in TRIM37-overexpressing Huh7 cells with or without PTEN overexpression. (E) WB analysis of EMT markers (Vimentin, E- and N-cadherin) in the same groups. Each experiment was repeated at least three independent biological replicates. Data are reported as mean ± SD (n=3). **, P<0.01; ***, P<0.001. CCK-8, Cell Counting Kit-8; EMT, epithelial-mesenchymal transition; HCC, hepatocellular carcinoma; SD, standard deviation; WB, Western blot.

Journal: Translational Cancer Research

Article Title: TRIM37 interacts with PTEN to promote progression of hepatocellular carcinoma cells by modulating AKT/GSK-3β/β-Catenin pathway

doi: 10.21037/tcr-2026-0447

Figure Lengend Snippet: TRIM37 facilitates HCC progression by inhibiting PTEN expression. (A) CCK-8 assessment was conducted to estimate the TRIM37-overexpressing Huh7 cell growth with or without PTEN upregulation. (B) Colony formation (crystal violet stained), and (C) Transwell invasion assessments were carried out to estimate the proliferative and invasive capabilities of TRIM37-upregulating Huh7 cells with or without PTEN upregulation (magnification ×200, crystal violet stained). (D) WB analysis of p-AKT, AKT, β-Catenin, p-GSK-3β, and GSK-3β expression in TRIM37-overexpressing Huh7 cells with or without PTEN overexpression. (E) WB analysis of EMT markers (Vimentin, E- and N-cadherin) in the same groups. Each experiment was repeated at least three independent biological replicates. Data are reported as mean ± SD (n=3). **, P<0.01; ***, P<0.001. CCK-8, Cell Counting Kit-8; EMT, epithelial-mesenchymal transition; HCC, hepatocellular carcinoma; SD, standard deviation; WB, Western blot.

Article Snippet: The tissue portions were subsequently treated with a primary antibody targeting TRIM37 (DF14825, Affinity Biosciences, 1:60) overnight at 4 °C after being blocked with 5% BSA for 30 min. Assays for TRIM37 detection were conducted with the use of 3,3'-diaminobenzidine (DAB) chromogen and secondary antibodies coupled with horseradish peroxidase (HRP).

Techniques: Expressing, CCK-8 Assay, Staining, Over Expression, Cell Counting, Standard Deviation, Western Blot