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Human Protein Atlas interactive survival plot and survival analysis
Interactive Survival Plot And Survival Analysis, supplied by Human Protein Atlas, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/interactive+survival+plot+and+survival+analysis/pmc12069594-305-4-10?v=Human+Protein+Atlas
Average 90 stars, based on 1 article reviews

interactive survival plot and survival analysis - by Bioz Stars, 2026-08

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Clinical and pathological information of colorectal cancer patients with low or high TRIM72 expression.

Journal: Heliyon

Article Title: TRIM72 inhibits cell migration and epithelial-mesenchymal transition by attenuating FAK/akt signaling in colorectal cancer

doi: 10.1016/j.heliyon.2024.e37714

Figure Lengend Snippet: Clinical and pathological information of colorectal cancer patients with low or high TRIM72 expression.

Article Snippet: The interactive survival scatter plot & Survival analysis data of TRIM72 in colorectal carcinoma are available via the human protein atlas database ( https://www.proteinatlas.org/ENSG00000177238-TRIM72/pathology/colorectal+cancer#ihc ).

Techniques: Expressing

TRIM72 is a potential prognostic indicator in patients with colorectal cancer. (A) TRIM72 expression is inversely related to tumor differentiation. Representative pictures of TRIM72 expression in normal and colon cancer patient tissue samples. Scale bar 50 mm (B) The relationship between TRIM72 expression and patient survival in our cohort. Low TRIM72 expression is associated with poor survival chances. (C, D) Analysis of colon cancer dataset on the human protein atlas database. Low TRIM72 expression is also linked to poor survival chances.

Journal: Heliyon

Article Title: TRIM72 inhibits cell migration and epithelial-mesenchymal transition by attenuating FAK/akt signaling in colorectal cancer

doi: 10.1016/j.heliyon.2024.e37714

Figure Lengend Snippet: TRIM72 is a potential prognostic indicator in patients with colorectal cancer. (A) TRIM72 expression is inversely related to tumor differentiation. Representative pictures of TRIM72 expression in normal and colon cancer patient tissue samples. Scale bar 50 mm (B) The relationship between TRIM72 expression and patient survival in our cohort. Low TRIM72 expression is associated with poor survival chances. (C, D) Analysis of colon cancer dataset on the human protein atlas database. Low TRIM72 expression is also linked to poor survival chances.

Techniques: Expressing

TRIM72 is underexpressed in metastatic colorectal cancer cells. (A) Real-time PCR analyses were performed to examine TRIM72 expression in primary colon tumor and paired liver metastases. (n = 10, P < 0.001) (B) Schematic representation of transwell invasion assay. (C) Colon cancer cells were seeded into the transwell membrane. After 24 h, the cells in the outer and inner part of the transwell membrane were collected and subjected to RT-PCR using TRIM72 primers.***P < 0.001, Data are presented as mean ± SD (n ≥ 3).

Journal: Heliyon

Article Title: TRIM72 inhibits cell migration and epithelial-mesenchymal transition by attenuating FAK/akt signaling in colorectal cancer

doi: 10.1016/j.heliyon.2024.e37714

Figure Lengend Snippet: TRIM72 is underexpressed in metastatic colorectal cancer cells. (A) Real-time PCR analyses were performed to examine TRIM72 expression in primary colon tumor and paired liver metastases. (n = 10, P < 0.001) (B) Schematic representation of transwell invasion assay. (C) Colon cancer cells were seeded into the transwell membrane. After 24 h, the cells in the outer and inner part of the transwell membrane were collected and subjected to RT-PCR using TRIM72 primers.***P < 0.001, Data are presented as mean ± SD (n ≥ 3).

Techniques: Real-time Polymerase Chain Reaction, Expressing, Transwell Invasion Assay, Membrane, Reverse Transcription Polymerase Chain Reaction

TRIM72 inhibits migration of colorectal cancer cells in vitro. (A, B) TRIM72 was overexpressed in two colon cancer cells, SW480 (A) and Lovo (B). The migration ability of the TRIM72 overexpression cells and the control cells was analyzed by wound healing. (C, D) Transwell migration assay for TRIM72 overexpression cells, SW480 (C) and Lovo (D). Twenty-four hours after seeding, the migrated cells were fixed, stained, and photographed. Scale bar, 100 μm (E) HCT116 TRIM72 knockout cells were established using CRISPR technique. The migration ability of the knockout and control cells was analyzed by wound healing. (F) Transwell migration assay for TRIM72 knockout cells, HCT116. Twenty-four hours after seeding, the migrated cells were fixed, stained and photographed. Scale bar, 100 μm *P < 0.05, ***P < 0.001, Data are presented as mean ± SD.

Journal: Heliyon

Article Title: TRIM72 inhibits cell migration and epithelial-mesenchymal transition by attenuating FAK/akt signaling in colorectal cancer

doi: 10.1016/j.heliyon.2024.e37714

Figure Lengend Snippet: TRIM72 inhibits migration of colorectal cancer cells in vitro. (A, B) TRIM72 was overexpressed in two colon cancer cells, SW480 (A) and Lovo (B). The migration ability of the TRIM72 overexpression cells and the control cells was analyzed by wound healing. (C, D) Transwell migration assay for TRIM72 overexpression cells, SW480 (C) and Lovo (D). Twenty-four hours after seeding, the migrated cells were fixed, stained, and photographed. Scale bar, 100 μm (E) HCT116 TRIM72 knockout cells were established using CRISPR technique. The migration ability of the knockout and control cells was analyzed by wound healing. (F) Transwell migration assay for TRIM72 knockout cells, HCT116. Twenty-four hours after seeding, the migrated cells were fixed, stained and photographed. Scale bar, 100 μm *P < 0.05, ***P < 0.001, Data are presented as mean ± SD.

Techniques: Migration, In Vitro, Over Expression, Control, Transwell Migration Assay, Staining, Knock-Out, CRISPR

TRIM72 restricts intravasation of colorectal cancer cells in embryonic Zebrafish. (A) SW480 colon cancer cells overexpressing TRIM72 or control plasmid were labelled with cell tracker and microinjected into zebrafish embryos. (B) HCT116 TRIM72 knockout or control cells were labelled with a cell tracker and microinjected into zebrafish embryos. Scale bar, 500 μm **P < 0.01, ***P < 0.001, Data are presented as mean ± SD (n ≥ 3).

Journal: Heliyon

Article Title: TRIM72 inhibits cell migration and epithelial-mesenchymal transition by attenuating FAK/akt signaling in colorectal cancer

doi: 10.1016/j.heliyon.2024.e37714

Figure Lengend Snippet: TRIM72 restricts intravasation of colorectal cancer cells in embryonic Zebrafish. (A) SW480 colon cancer cells overexpressing TRIM72 or control plasmid were labelled with cell tracker and microinjected into zebrafish embryos. (B) HCT116 TRIM72 knockout or control cells were labelled with a cell tracker and microinjected into zebrafish embryos. Scale bar, 500 μm **P < 0.01, ***P < 0.001, Data are presented as mean ± SD (n ≥ 3).

Techniques: Control, Plasmid Preparation, Knock-Out

TRIM72 suppresses EMT progression of colorectal cancer cells by attenuating FAK/Akt signaling pathway. (A) Western blot assay was used to determine the expression of E-cadherin, N-cadherin, and vimentin, in SW480 colon cancer cells overexpressing TRIM72, or control plasmid. Quantitation of relevant protein levels were shown in right pane (n.s., not significant; *P < 0.05, **P < 0.01, ***P < 0.001; n = 3). (B) Western blot assay was used to determine the expression of E-cadherin, N-cadherin, and vimentin in HCT116 TRIM72 knockout or control cells. Quantitation of relevant protein levels were shown in right pane (n.s., not significant; *P < 0.05, **P < 0.01, ***P < 0.001; n = 3). (C) Circulating tumor cells were isolated from colon cancer patients, and the expression of TRIM72, vimentin and other marker was determined using immunofluorescence. (D) Co-immunoprecipitation of TRIM72 and FAK proteins in two colon cancer cells, SW480 and HCT116. (E) Western blot assay was used to determine the expression of FAK, AKT, and p-AKT in TRIM72 overexpression cells treated with or without mg132. (F) 293T cells were co-transfected with Myc-FAK, Myc-TRIM72, Ub-Ha as shown for 24 h and subsequently treated with or without MG132 for 12 h. The cells were lysed and subjected to IP with anti-Myc-conjugated beads. The immunoprecipitated proteins were subjected to western analysis using the indicated antibodies.

Journal: Heliyon

Article Title: TRIM72 inhibits cell migration and epithelial-mesenchymal transition by attenuating FAK/akt signaling in colorectal cancer

doi: 10.1016/j.heliyon.2024.e37714

Figure Lengend Snippet: TRIM72 suppresses EMT progression of colorectal cancer cells by attenuating FAK/Akt signaling pathway. (A) Western blot assay was used to determine the expression of E-cadherin, N-cadherin, and vimentin, in SW480 colon cancer cells overexpressing TRIM72, or control plasmid. Quantitation of relevant protein levels were shown in right pane (n.s., not significant; *P < 0.05, **P < 0.01, ***P < 0.001; n = 3). (B) Western blot assay was used to determine the expression of E-cadherin, N-cadherin, and vimentin in HCT116 TRIM72 knockout or control cells. Quantitation of relevant protein levels were shown in right pane (n.s., not significant; *P < 0.05, **P < 0.01, ***P < 0.001; n = 3). (C) Circulating tumor cells were isolated from colon cancer patients, and the expression of TRIM72, vimentin and other marker was determined using immunofluorescence. (D) Co-immunoprecipitation of TRIM72 and FAK proteins in two colon cancer cells, SW480 and HCT116. (E) Western blot assay was used to determine the expression of FAK, AKT, and p-AKT in TRIM72 overexpression cells treated with or without mg132. (F) 293T cells were co-transfected with Myc-FAK, Myc-TRIM72, Ub-Ha as shown for 24 h and subsequently treated with or without MG132 for 12 h. The cells were lysed and subjected to IP with anti-Myc-conjugated beads. The immunoprecipitated proteins were subjected to western analysis using the indicated antibodies.

Techniques: Western Blot, Expressing, Control, Plasmid Preparation, Quantitation Assay, Knock-Out, Isolation, Marker, Immunofluorescence, Immunoprecipitation, Over Expression, Transfection