mst4 antibody  (Santa Cruz Biotechnology)

Journal: Cellular and Molecular Gastroenterology and Hepatology

Article Title: Therapeutic Potential of STE20-Type Kinase STK25 Inhibition for the Prevention and Treatment of Metabolically Induced Hepatocellular Carcinoma

doi: 10.1016/j.jcmgh.2025.101485

Figure Lengend Snippet: List of Antibodies Used for Western Blot, Immunohistochemical/Immunofluorescence Analysis, and Flow Cytometry

Article Snippet: , anti-MST4 (#3822) anti-GAPDH (sc-47724) anti-vinculin (sc-25336) , 1:1000 1:1000 1:500 , Cell Signaling Technology Santa Cruz Biotechnology Santa Cruz Biotechnology.

Techniques: Western Blot, Immunohistochemical staining, Plasmid Preparation

Journal: Translational Oncology

Article Title: Targeting STK26 and ATG4B: miR-22-3p as a modulator of autophagy and tumor progression in HCC

doi: 10.1016/j.tranon.2024.102214

Figure Lengend Snippet: Details regarding the primers, plasmids, drug reagents, and antibodies employed in the experimental procedure

Article Snippet: Antibody(WB) , STK26 , Proteintech Group, Inc;Cat No.10847-1-AP (1:1000).

Techniques: Sequencing, Plasmid Preparation

Journal: Translational Oncology

Article Title: Targeting STK26 and ATG4B: miR-22-3p as a modulator of autophagy and tumor progression in HCC

doi: 10.1016/j.tranon.2024.102214

Figure Lengend Snippet: miR-22-3p is downregulated in hepatocellular carcinoma and associated with poor prognosis. (A) Analysis using the TCGA database revealed that miR-22-3p expression is significantly reduced in breast cancer, cholangiocarcinoma, hepatocellular carcinoma, pheochromocytoma, and paraganglioma. (B) miR-22-3p expression is significantly downregulated in hepatocellular carcinoma. (C) Paired analysis showed that miR-22-3p expression is significantly lower in hepatocellular carcinoma tissues compared to corresponding normal tissues. (D) Survival curve analysis indicated that patients with low miR-22-3p expression have significantly shorter overall survival (OS). (E) Real-time PCR analysis of miR-22-3p expression in the normal liver cell line THLE-2 and five hepatocellular carcinoma cell lines. (F) Real-time PCR analysis of STK26 expression in hepatocellular carcinoma tumor tissues and adjacent non-tumor tissues. (G) Real-time PCR analysis of miR-22-3p expression in HCCLM3 and SNU398 cells following transfection with miR-22-3p mimic. Data are presented as mean ± standard deviation of three independent experiments. Significant differences compared to the control group: *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.

Article Snippet: Antibody(WB) , STK26 , Proteintech Group, Inc;Cat No.10847-1-AP (1:1000).

Techniques: Expressing, Real-time Polymerase Chain Reaction, Transfection, Standard Deviation, Control

Journal: Translational Oncology

Article Title: Targeting STK26 and ATG4B: miR-22-3p as a modulator of autophagy and tumor progression in HCC

doi: 10.1016/j.tranon.2024.102214

Figure Lengend Snippet: miR-22-3p inhibits HCC cell proliferation and autophagy in vitro. (A) EDU assay assessing proliferation of HCCLM3 and SNU398 cells following transfection with miR-22-3p mimic and inhibitor. (B) Scratch assay evaluating the effect of miR-22-3p on HCC cell migration. (C) Transwell assay analyzing the impact of miR-22-3p on HCC cell invasion. (D) Western blot analysis of autophagy-related proteins LC3B, P62, and STK26, ATG4B, and p-ATG4B (Ser383) in cells transfected with miR-22-3p mimic and inhibitor. (E) After transfecting HCCLM3 cells with miR-22-3p, autophagic flux was assessed using the LC3B dual-reporter system (mRFP1-EGFP-LC3B). Yellow puncta indicate autophagosomes, while red puncta represent the fusion of autophagosomes with lysosomes. Data are presented as mean ± standard deviation of three independent experiments. Significant differences compared to the control group: *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.

Article Snippet: Antibody(WB) , STK26 , Proteintech Group, Inc;Cat No.10847-1-AP (1:1000).

Techniques: In Vitro, EdU Assay, Transfection, Wound Healing Assay, Migration, Transwell Assay, Western Blot, Standard Deviation, Control

Journal: Translational Oncology

Article Title: Targeting STK26 and ATG4B: miR-22-3p as a modulator of autophagy and tumor progression in HCC

doi: 10.1016/j.tranon.2024.102214

Figure Lengend Snippet: miR-22-3p enhances sorafenib-induced hepatocellular carcinoma cell death by regulating autophagy. (A) Western blot analysis of the effects of different concentrations of sorafenib (0-20μM) on the expression of STK26, ATG4B, p-ATG4B, autophagy marker protein LC3B, and P62, along with an evaluation of autophagic flux using the LC3B double reporter (mRFP1-EGFP-LC3B) (B). (C) Flow cytometry analysis of the effects of miR-22-3p and sorafenib on hepatocellular carcinoma cell apoptosis.In vivo experiments in nude mice injected with HCCLM3 cells stably expressing miR-22-3p and treated with sorafenib: (D) Photographs of tumor tissues, (E) Tumor growth curves and weight records, (F) Immunohistochemistry (IHC) analysis of STK26, ATG4B, and Ki-67 expression in tumor tissues. All data are presented as mean ± standard deviation of three independent experiments. Significant differences compared to the control group: *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001.

Article Snippet: Antibody(WB) , STK26 , Proteintech Group, Inc;Cat No.10847-1-AP (1:1000).

Techniques: Western Blot, Expressing, Marker, Flow Cytometry, In Vivo, Injection, Stable Transfection, Immunohistochemistry, Standard Deviation, Control

Journal: Translational Oncology

Article Title: Targeting STK26 and ATG4B: miR-22-3p as a modulator of autophagy and tumor progression in HCC

doi: 10.1016/j.tranon.2024.102214

Figure Lengend Snippet: miR-22-3p targets and regulates STK26 and ATG4B. (A) Bioinformatic prediction using miRanda and TargetScan identified miR-22-3p as the only miRNA targeting both STK26 and ATG4B. (B) miR-22-3p shares common binding sites in the 3′UTR of STK26 and ATG4B. (C) Analysis of the TCGA database showed a significant negative correlation between miR-22-3p and the expression of STK26 and ATG4B, while STK26 and ATG4B expression was positively correlated. (D) Wild-type and mutant dual-luciferase reporter gene plasmids were constructed for STK26-3′UTR and ATG4B-3′UTR. Transfection with miR-22-3p mimic significantly reduced the fluorescence intensity of the wild-type STK26-3′UTR and ATG4B-3′UTR. Data are presented as mean ± standard deviation of three independent experiments. Significant differences compared to the control group: *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.

Article Snippet: Antibody(WB) , STK26 , Proteintech Group, Inc;Cat No.10847-1-AP (1:1000).

Techniques: Binding Assay, Expressing, Mutagenesis, Luciferase, Construct, Transfection, Fluorescence, Standard Deviation, Control

Journal: Translational Oncology

Article Title: Targeting STK26 and ATG4B: miR-22-3p as a modulator of autophagy and tumor progression in HCC

doi: 10.1016/j.tranon.2024.102214

Figure Lengend Snippet: STK26 is highly expressed in hepatocellular carcinoma and closely associated with poor prognosis. (A) TCGA database analysis revealed that STK26 is upregulated in various cancers, including breast cancer, colorectal adenocarcinoma, cholangiocarcinoma, esophageal carcinoma, head and neck squamous cell carcinoma, hepatocellular carcinoma, lung squamous cell carcinoma, and gastric adenocarcinoma. (B) STK26 expression is significantly higher in hepatocellular carcinoma tissues compared to non-tumor tissues. (C) Paired tumor samples from hepatocellular carcinoma patients showed significant upregulation of STK26. (D) Kaplan-Meier survival analysis indicated that high STK26 expression is associated with significantly shorter overall survival in hepatocellular carcinoma patients. (E) UALCAN database analysis showed changes in STK26 promoter methylation levels. (F) Western blot analysis of STK26 expression in THLE-2, HUH-7, HCCLM3, SNU398, and Hep3B cell lines. (G) Immunohistochemistry (IHC) analysis of STK26 expression in hepatocellular carcinoma and adjacent non-tumor tissues. Data are presented as mean ± standard deviation of three independent experiments. Significant differences compared to the control group: *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.

Article Snippet: Antibody(WB) , STK26 , Proteintech Group, Inc;Cat No.10847-1-AP (1:1000).

Techniques: Expressing, Methylation, Western Blot, Immunohistochemistry, Standard Deviation, Control

Journal: Translational Oncology

Article Title: Targeting STK26 and ATG4B: miR-22-3p as a modulator of autophagy and tumor progression in HCC

doi: 10.1016/j.tranon.2024.102214

Figure Lengend Snippet: STK26 promotes hepatocellular carcinoma cell proliferation, migration, and invasion. (A) Knockdown and overexpression of STK26 were performed in HCCLM3 and SNU398 cells using three different sh-STK26 and pcDNA3.1-STK26 plasmids, with Western blot analysis confirming knockdown and overexpression efficiency. (B) EDU assay assessing cell proliferation, (C) Scratch healing assay evaluating cell migration, (D) Transwell invasion assay assessing the impact of STK26 on hepatocellular carcinoma cell invasion. Data are presented as mean ± standard deviation of three independent experiments. Significant differences compared to the control group: *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.

Article Snippet: Antibody(WB) , STK26 , Proteintech Group, Inc;Cat No.10847-1-AP (1:1000).

Techniques: Migration, Knockdown, Over Expression, Western Blot, EdU Assay, Transwell Invasion Assay, Standard Deviation, Control

Journal: Translational Oncology

Article Title: Targeting STK26 and ATG4B: miR-22-3p as a modulator of autophagy and tumor progression in HCC

doi: 10.1016/j.tranon.2024.102214

Figure Lengend Snippet: STK26 promotes hepatocellular carcinoma growth and autophagy in vivo. Using STK26 knockdown HCCLM3 cells in a nude mouse xenograft model: (A) Photographs of tumor tissues, (B) Tumor growth curves, (C) Tumor weight records, (D) Immunohistochemistry (IHC) analysis of STK26 and Ki-67 protein expression in tumor tissues. (E) Western blot analysis of autophagy-related proteins LC3B, P62, STK26, ATG4B, and p-ATG4B (Ser383). (F)Autophagic flux was assessed in HCCLM3 cells using the LC3B dual-reporter system (mRFP1-EGFP-LC3B). Data are presented as mean ± standard deviation of three independent experiments. Significant differences compared to the control group: *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.

Article Snippet: Antibody(WB) , STK26 , Proteintech Group, Inc;Cat No.10847-1-AP (1:1000).

Techniques: In Vivo, Knockdown, Immunohistochemistry, Expressing, Western Blot, Standard Deviation, Control

Journal: Translational Oncology

Article Title: Targeting STK26 and ATG4B: miR-22-3p as a modulator of autophagy and tumor progression in HCC

doi: 10.1016/j.tranon.2024.102214

Figure Lengend Snippet: miR-22-3p regulates STK26 to inhibit cell proliferation, migration, and invasion. (A) EDU assay assessing cell proliferation, (B) Scratch assay evaluating cell migration, (C) Transwell chamber assay analyzing cell invasion. (D) Western blot analysis of STK26, P62, p-ATG4B, GAPDH, and LC3II/I protein expression. (E) Evaluation of autophagic flux in HCC cells using the LC3B double reporter (mRFP1-EGFP-LC3B). All data are presented as mean ± standard deviation of three independent experiments. Significant differences compared to the control group: *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001.

Article Snippet: Antibody(WB) , STK26 , Proteintech Group, Inc;Cat No.10847-1-AP (1:1000).

Techniques: Migration, EdU Assay, Wound Healing Assay, Transwell Chamber Assay, Western Blot, Expressing, Standard Deviation, Control