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gv493 short hairpin rna sh plasmid targeting upk1b  (Genechem)

 
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    Structured Review

    Genechem gv493 short hairpin rna sh plasmid targeting upk1b
    Metastasis-related 12-gene signature, and identification of <t>UPK1B</t> and CGB5 as independent prognostic markers associated with advanced metastatic GC. (A) Venn diagram showing the intersection of genes upregulated in N1-3 stage and M1 stage GC tissues. (B) LASSO Cox regression analysis based on TCGA-STAD data identified a metastasis-associated prognostic risk signature. LASSO coefficient profiles of the signature genes in the merged dataset are shown (top) and the coefficient profile plot is generated against the log(λ) sequence (bottom). (C) The high-risk group of patients with GC exhibited a poor prognosis (overall survival). High expression of (D) CGB5 and (E) UPK1B was associated with poor overall survival in patients with GC based on data from the TCGA-STAD cohort. (F) Elevated UPK1B expression predicted poor prognosis (overall survival) of patients with GC in the Kaplan-Meier plotter database. UPK1B expression was increased in (G) M1 compared with M0 and in (H) N2 metastatic stage GC tissues compared with N0 stage. UPK1B, uroplakin 1B; CGB5, chorionic gonadotropin subunit β-5; GC, gastric cancer; LASSO, Least Absolute Shrinkage and Selection Operator; TCGA-STAD, The Cancer Genome Atlas Stomach Adenocarcinoma; HR, hazard ratio; TPM, transcripts per million.
    Gv493 Short Hairpin Rna Sh Plasmid Targeting Upk1b, supplied by Genechem, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/gv493+plasmid/hairpin+rna+short/pmc13203321-46-9-29
    Average 86 stars, based on 1 article reviews
    gv493 short hairpin rna sh plasmid targeting upk1b - by Bioz Stars, 2026-10
    86/100 stars

    Images

    1) Product Images from "CDX2-UPK1B-PIK3IP1-PI3K/AKT signaling axis regulates gastric cancer cell invasion and migration and influences patient prognosis"

    Article Title: CDX2-UPK1B-PIK3IP1-PI3K/AKT signaling axis regulates gastric cancer cell invasion and migration and influences patient prognosis

    Journal: Experimental and Therapeutic Medicine

    doi: 10.3892/etm.2026.13179

    Metastasis-related 12-gene signature, and identification of UPK1B and CGB5 as independent prognostic markers associated with advanced metastatic GC. (A) Venn diagram showing the intersection of genes upregulated in N1-3 stage and M1 stage GC tissues. (B) LASSO Cox regression analysis based on TCGA-STAD data identified a metastasis-associated prognostic risk signature. LASSO coefficient profiles of the signature genes in the merged dataset are shown (top) and the coefficient profile plot is generated against the log(λ) sequence (bottom). (C) The high-risk group of patients with GC exhibited a poor prognosis (overall survival). High expression of (D) CGB5 and (E) UPK1B was associated with poor overall survival in patients with GC based on data from the TCGA-STAD cohort. (F) Elevated UPK1B expression predicted poor prognosis (overall survival) of patients with GC in the Kaplan-Meier plotter database. UPK1B expression was increased in (G) M1 compared with M0 and in (H) N2 metastatic stage GC tissues compared with N0 stage. UPK1B, uroplakin 1B; CGB5, chorionic gonadotropin subunit β-5; GC, gastric cancer; LASSO, Least Absolute Shrinkage and Selection Operator; TCGA-STAD, The Cancer Genome Atlas Stomach Adenocarcinoma; HR, hazard ratio; TPM, transcripts per million.
    Figure Legend Snippet: Metastasis-related 12-gene signature, and identification of UPK1B and CGB5 as independent prognostic markers associated with advanced metastatic GC. (A) Venn diagram showing the intersection of genes upregulated in N1-3 stage and M1 stage GC tissues. (B) LASSO Cox regression analysis based on TCGA-STAD data identified a metastasis-associated prognostic risk signature. LASSO coefficient profiles of the signature genes in the merged dataset are shown (top) and the coefficient profile plot is generated against the log(λ) sequence (bottom). (C) The high-risk group of patients with GC exhibited a poor prognosis (overall survival). High expression of (D) CGB5 and (E) UPK1B was associated with poor overall survival in patients with GC based on data from the TCGA-STAD cohort. (F) Elevated UPK1B expression predicted poor prognosis (overall survival) of patients with GC in the Kaplan-Meier plotter database. UPK1B expression was increased in (G) M1 compared with M0 and in (H) N2 metastatic stage GC tissues compared with N0 stage. UPK1B, uroplakin 1B; CGB5, chorionic gonadotropin subunit β-5; GC, gastric cancer; LASSO, Least Absolute Shrinkage and Selection Operator; TCGA-STAD, The Cancer Genome Atlas Stomach Adenocarcinoma; HR, hazard ratio; TPM, transcripts per million.

    Techniques Used: Generated, Sequencing, Expressing, Selection

    UPK1B drives GC cell invasion and migration in a PI3K/AKT-dependent manner. (A) Gene set enrichment analysis indicated that genes upregulated in the UPK1B-high group were enriched in the PI3K/AKT pathway. (B) Protein levels of UPK1B in GC cell lines. (C) Knockdown of UPK1B reduced PI3K/AKT activation in MKN45 cells. Silencing UPK1B suppressed the (D) migration/invasion capacity and (E) wound closure rate of MKN45 cells. (F) Overexpression of UPK1B enhanced PI3K/AKT pathway activation in AGS cells, which was attenuated by the PI3K inhibitor LY294002. Inhibition of PI3K/AKT signaling reversed UPK1B-induced (G) migration/invasion capacity and (H) wound closure rate of AGS cells. UPK1B, uroplakin 1B; GC, gastric cancer; p-, phosphorylated; sh, short hairpin RNA; NC, negative control; OE, overexpression.
    Figure Legend Snippet: UPK1B drives GC cell invasion and migration in a PI3K/AKT-dependent manner. (A) Gene set enrichment analysis indicated that genes upregulated in the UPK1B-high group were enriched in the PI3K/AKT pathway. (B) Protein levels of UPK1B in GC cell lines. (C) Knockdown of UPK1B reduced PI3K/AKT activation in MKN45 cells. Silencing UPK1B suppressed the (D) migration/invasion capacity and (E) wound closure rate of MKN45 cells. (F) Overexpression of UPK1B enhanced PI3K/AKT pathway activation in AGS cells, which was attenuated by the PI3K inhibitor LY294002. Inhibition of PI3K/AKT signaling reversed UPK1B-induced (G) migration/invasion capacity and (H) wound closure rate of AGS cells. UPK1B, uroplakin 1B; GC, gastric cancer; p-, phosphorylated; sh, short hairpin RNA; NC, negative control; OE, overexpression.

    Techniques Used: Migration, Knockdown, Activation Assay, Over Expression, Inhibition, shRNA, Negative Control

    CDX2 acts as a transcriptional repressor of UPK1B and its high expression is associated with favorable prognosis of patients with GC. (A) Venn diagram showing overlapping predicted transcriptional regulators of UPK1B from ChEA and ChEA3 databases. (B) Knockdown of CDX2 in AGS cells resulted in increased UPK1B (C) mRNA and (D) protein expression. (E) Overexpression of CDX2 in MKN45 cells reduced UPK1B protein levels. Data from (F) The Cancer Genome Atlas Stomach Adenocarcinoma cohort and (G) the Kaplan-Meier plotter database indicated that high CDX2 expression was associated with improved prognosis of patients with GC. UPK1B, uroplakin 1B; GC, gastric cancer; si, small interfering RNA; NC, negative control; OE, overexpression; HR, hazard ratio; CDX2, caudal-related homeobox transcription factor 2; ChEA, ChIP-X Enrichment Analysis.
    Figure Legend Snippet: CDX2 acts as a transcriptional repressor of UPK1B and its high expression is associated with favorable prognosis of patients with GC. (A) Venn diagram showing overlapping predicted transcriptional regulators of UPK1B from ChEA and ChEA3 databases. (B) Knockdown of CDX2 in AGS cells resulted in increased UPK1B (C) mRNA and (D) protein expression. (E) Overexpression of CDX2 in MKN45 cells reduced UPK1B protein levels. Data from (F) The Cancer Genome Atlas Stomach Adenocarcinoma cohort and (G) the Kaplan-Meier plotter database indicated that high CDX2 expression was associated with improved prognosis of patients with GC. UPK1B, uroplakin 1B; GC, gastric cancer; si, small interfering RNA; NC, negative control; OE, overexpression; HR, hazard ratio; CDX2, caudal-related homeobox transcription factor 2; ChEA, ChIP-X Enrichment Analysis.

    Techniques Used: Expressing, Knockdown, Over Expression, Small Interfering RNA, Negative Control

    UPK1B activates PI3K/AKT signaling by antagonizing the inhibitory regulator PIK3IP1 in gastric cancer cells. (A) Venn diagram showing that PIK3IP1 was identified as a putative UPK1B-interacting partner based on BioGRID and HIPPIE protein-protein interaction databases. (B) UPK1B and PIK3IP1 co-localized in the cytoplasm and plasma membrane of MKN45 cells. (C) Interaction between UPK1B and PIK3IP1 in MKN45 cells. (D) Knockdown of PIK3IP1 in MKN45 cells. (E) Silencing PIK3IP1 in UPK1B-knockdown MKN45 cells restored PI3K/AKT pathway activation. Knockdown of PIK3IP1 reversed the decrease in (F) migration/invasion and (G) wound-healing capacity in UPK1B-silenced MKN45 cells. UPK1B, uroplakin 1B; p-, phosphorylated; si, small interfering RNA; sh, short hairpin RNA; NC, negative control; PIK3IP1, PI3K inhibitor interacting protein 1; HIPPIE, Human Integrated Protein-Protein Interaction Reference; IP, immunoprecipitation.
    Figure Legend Snippet: UPK1B activates PI3K/AKT signaling by antagonizing the inhibitory regulator PIK3IP1 in gastric cancer cells. (A) Venn diagram showing that PIK3IP1 was identified as a putative UPK1B-interacting partner based on BioGRID and HIPPIE protein-protein interaction databases. (B) UPK1B and PIK3IP1 co-localized in the cytoplasm and plasma membrane of MKN45 cells. (C) Interaction between UPK1B and PIK3IP1 in MKN45 cells. (D) Knockdown of PIK3IP1 in MKN45 cells. (E) Silencing PIK3IP1 in UPK1B-knockdown MKN45 cells restored PI3K/AKT pathway activation. Knockdown of PIK3IP1 reversed the decrease in (F) migration/invasion and (G) wound-healing capacity in UPK1B-silenced MKN45 cells. UPK1B, uroplakin 1B; p-, phosphorylated; si, small interfering RNA; sh, short hairpin RNA; NC, negative control; PIK3IP1, PI3K inhibitor interacting protein 1; HIPPIE, Human Integrated Protein-Protein Interaction Reference; IP, immunoprecipitation.

    Techniques Used: Clinical Proteomics, Membrane, Knockdown, Activation Assay, Migration, Small Interfering RNA, shRNA, Negative Control, Immunoprecipitation

    Related Articles

    Amplification:

    Article Title: P2Y12 receptor as a new target for electroacupuncture relieving comorbidity of visceral pain and depression of inflammatory bowel disease
    Article Snippet: .. We amplified the shRNA coding sequence of P2Y12 by reverse transcription polymerase chain reaction and ligated it into the GV493 plasmid to generate LV-P2ry12-RNAi (Shanghai Genechem Co., Shanghai, China), and LV-GFP was used as a control. ..

    shRNA:

    Article Title: P2Y12 receptor as a new target for electroacupuncture relieving comorbidity of visceral pain and depression of inflammatory bowel disease
    Article Snippet: .. We amplified the shRNA coding sequence of P2Y12 by reverse transcription polymerase chain reaction and ligated it into the GV493 plasmid to generate LV-P2ry12-RNAi (Shanghai Genechem Co., Shanghai, China), and LV-GFP was used as a control. ..

    Article Title: Bile acids activate cancer-associated fibroblasts and induce an immunosuppressive microenvironment in cholangiocarcinoma.
    Article Snippet: In brief Huang et al. reveal that high bile acid levels in the cholangiocarcinoma tumor microenvironment activate GPBAR1 on cancer-associated fibroblasts, inducing CXCL10 secretion.. This recruits neutrophils and maintains their immature phenotype, thereby potentiating immunosuppression.. Targeting GPBAR1 or CXCL10 enhances pembrolizumab response, offering a potential strategy to improve cholangiocarcinoma immunotherapy efficacy.

    Article Title: Homocysteine Impairs Endothelial Cell Barrier Function and Angiogenic Potential via the Progranulin/EphA2 Pathway.
    Article Snippet: .. EphA2 knockdown was performed by transfecting cells with EphA2 (NM_004431) shRNA, which was inserted into the GV493 plasmid according to the instructions of GENEChem. ..

    Sequencing:

    Article Title: P2Y12 receptor as a new target for electroacupuncture relieving comorbidity of visceral pain and depression of inflammatory bowel disease
    Article Snippet: .. We amplified the shRNA coding sequence of P2Y12 by reverse transcription polymerase chain reaction and ligated it into the GV493 plasmid to generate LV-P2ry12-RNAi (Shanghai Genechem Co., Shanghai, China), and LV-GFP was used as a control. ..

    Article Title: Role of mu-opioid receptor in nociceptive modulation in anterior cingulate cortex of rats
    Article Snippet: .. The green fluorescent protein-reporting lentivirus encoding the siRNA targeting MOR and MOR meaningless sequence were custom-constructed into the GV493 plasmid by Shanghai GeneChem. .. Vector titer (viral particles per milliliter) was determined by dot-blot hybridization analysis.

    Reverse Transcription:

    Article Title: P2Y12 receptor as a new target for electroacupuncture relieving comorbidity of visceral pain and depression of inflammatory bowel disease
    Article Snippet: .. We amplified the shRNA coding sequence of P2Y12 by reverse transcription polymerase chain reaction and ligated it into the GV493 plasmid to generate LV-P2ry12-RNAi (Shanghai Genechem Co., Shanghai, China), and LV-GFP was used as a control. ..

    Polymerase Chain Reaction:

    Article Title: P2Y12 receptor as a new target for electroacupuncture relieving comorbidity of visceral pain and depression of inflammatory bowel disease
    Article Snippet: .. We amplified the shRNA coding sequence of P2Y12 by reverse transcription polymerase chain reaction and ligated it into the GV493 plasmid to generate LV-P2ry12-RNAi (Shanghai Genechem Co., Shanghai, China), and LV-GFP was used as a control. ..

    Plasmid Preparation:

    Article Title: P2Y12 receptor as a new target for electroacupuncture relieving comorbidity of visceral pain and depression of inflammatory bowel disease
    Article Snippet: .. We amplified the shRNA coding sequence of P2Y12 by reverse transcription polymerase chain reaction and ligated it into the GV493 plasmid to generate LV-P2ry12-RNAi (Shanghai Genechem Co., Shanghai, China), and LV-GFP was used as a control. ..

    Article Title: FUCA2 Is a Prognostic Biomarker and Correlated With an Immunosuppressive Microenvironment in Pan-Cancer
    Article Snippet: Statistical analyses were performed with GraphPad Prism. .. The siRNAs for FUCA2 (NM_032020) were ligated into the GV493 plasmid (GeneChem). ..

    Article Title: Role of mu-opioid receptor in nociceptive modulation in anterior cingulate cortex of rats
    Article Snippet: .. The green fluorescent protein-reporting lentivirus encoding the siRNA targeting MOR and MOR meaningless sequence were custom-constructed into the GV493 plasmid by Shanghai GeneChem. .. Vector titer (viral particles per milliliter) was determined by dot-blot hybridization analysis.

    Article Title: Bile acids activate cancer-associated fibroblasts and induce an immunosuppressive microenvironment in cholangiocarcinoma.
    Article Snippet: In brief Huang et al. reveal that high bile acid levels in the cholangiocarcinoma tumor microenvironment activate GPBAR1 on cancer-associated fibroblasts, inducing CXCL10 secretion.. This recruits neutrophils and maintains their immature phenotype, thereby potentiating immunosuppression.. Targeting GPBAR1 or CXCL10 enhances pembrolizumab response, offering a potential strategy to improve cholangiocarcinoma immunotherapy efficacy.

    Article Title: Homocysteine Impairs Endothelial Cell Barrier Function and Angiogenic Potential via the Progranulin/EphA2 Pathway.
    Article Snippet: .. EphA2 knockdown was performed by transfecting cells with EphA2 (NM_004431) shRNA, which was inserted into the GV493 plasmid according to the instructions of GENEChem. ..

    Article Title: LPCAT1 , the Enzyme Responsible for Converting LPC to PC , Promotes OPC Differentiation In Vitro
    Article Snippet: .. It was ligated into the GV493 plasmid (GeneChem, Shanghai, China). .. The LPCAT1 over‐expressing lentivirus was also constructed by GeneChem.

    Article Title: LPCAT1, the Enzyme Responsible for Converting LPC to PC, Promotes OPC Differentiation In Vitro.
    Article Snippet: .. It was ligated into the GV493 plasmid (GeneChem, Shanghai, China). .. The LPCAT1 over- expressing lentivirus was also constructed by GeneChem.

    Control:

    Article Title: P2Y12 receptor as a new target for electroacupuncture relieving comorbidity of visceral pain and depression of inflammatory bowel disease
    Article Snippet: .. We amplified the shRNA coding sequence of P2Y12 by reverse transcription polymerase chain reaction and ligated it into the GV493 plasmid to generate LV-P2ry12-RNAi (Shanghai Genechem Co., Shanghai, China), and LV-GFP was used as a control. ..

    Stable Transfection:

    Article Title: Bile acids activate cancer-associated fibroblasts and induce an immunosuppressive microenvironment in cholangiocarcinoma.
    Article Snippet: In brief Huang et al. reveal that high bile acid levels in the cholangiocarcinoma tumor microenvironment activate GPBAR1 on cancer-associated fibroblasts, inducing CXCL10 secretion.. This recruits neutrophils and maintains their immature phenotype, thereby potentiating immunosuppression.. Targeting GPBAR1 or CXCL10 enhances pembrolizumab response, offering a potential strategy to improve cholangiocarcinoma immunotherapy efficacy.

    Clone Assay:

    Article Title: Bile acids activate cancer-associated fibroblasts and induce an immunosuppressive microenvironment in cholangiocarcinoma.
    Article Snippet: In brief Huang et al. reveal that high bile acid levels in the cholangiocarcinoma tumor microenvironment activate GPBAR1 on cancer-associated fibroblasts, inducing CXCL10 secretion.. This recruits neutrophils and maintains their immature phenotype, thereby potentiating immunosuppression.. Targeting GPBAR1 or CXCL10 enhances pembrolizumab response, offering a potential strategy to improve cholangiocarcinoma immunotherapy efficacy.

    other:

    Article Title: Suppression of non-muscle myosin II boosts T cell cytotoxicity against tumors
    Article Snippet: Both GV493 and GV248 plasmids are from Shanghai Genechem Co. Ltd. Ble, Lat, Jas, trichostatin A (TSA), and ML7 were bought from Selleck Chemicals.

    Knockdown:

    Article Title: Homocysteine Impairs Endothelial Cell Barrier Function and Angiogenic Potential via the Progranulin/EphA2 Pathway.
    Article Snippet: .. EphA2 knockdown was performed by transfecting cells with EphA2 (NM_004431) shRNA, which was inserted into the GV493 plasmid according to the instructions of GENEChem. ..



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    Metastasis-related 12-gene signature, and identification of UPK1B and CGB5 as independent prognostic markers associated with advanced metastatic GC. (A) Venn diagram showing the intersection of genes upregulated in N1-3 stage and M1 stage GC tissues. (B) LASSO Cox regression analysis based on TCGA-STAD data identified a metastasis-associated prognostic risk signature. LASSO coefficient profiles of the signature genes in the merged dataset are shown (top) and the coefficient profile plot is generated against the log(λ) sequence (bottom). (C) The high-risk group of patients with GC exhibited a poor prognosis (overall survival). High expression of (D) CGB5 and (E) UPK1B was associated with poor overall survival in patients with GC based on data from the TCGA-STAD cohort. (F) Elevated UPK1B expression predicted poor prognosis (overall survival) of patients with GC in the Kaplan-Meier plotter database. UPK1B expression was increased in (G) M1 compared with M0 and in (H) N2 metastatic stage GC tissues compared with N0 stage. UPK1B, uroplakin 1B; CGB5, chorionic gonadotropin subunit β-5; GC, gastric cancer; LASSO, Least Absolute Shrinkage and Selection Operator; TCGA-STAD, The Cancer Genome Atlas Stomach Adenocarcinoma; HR, hazard ratio; TPM, transcripts per million.

    Journal: Experimental and Therapeutic Medicine

    Article Title: CDX2-UPK1B-PIK3IP1-PI3K/AKT signaling axis regulates gastric cancer cell invasion and migration and influences patient prognosis

    doi: 10.3892/etm.2026.13179

    Figure Lengend Snippet: Metastasis-related 12-gene signature, and identification of UPK1B and CGB5 as independent prognostic markers associated with advanced metastatic GC. (A) Venn diagram showing the intersection of genes upregulated in N1-3 stage and M1 stage GC tissues. (B) LASSO Cox regression analysis based on TCGA-STAD data identified a metastasis-associated prognostic risk signature. LASSO coefficient profiles of the signature genes in the merged dataset are shown (top) and the coefficient profile plot is generated against the log(λ) sequence (bottom). (C) The high-risk group of patients with GC exhibited a poor prognosis (overall survival). High expression of (D) CGB5 and (E) UPK1B was associated with poor overall survival in patients with GC based on data from the TCGA-STAD cohort. (F) Elevated UPK1B expression predicted poor prognosis (overall survival) of patients with GC in the Kaplan-Meier plotter database. UPK1B expression was increased in (G) M1 compared with M0 and in (H) N2 metastatic stage GC tissues compared with N0 stage. UPK1B, uroplakin 1B; CGB5, chorionic gonadotropin subunit β-5; GC, gastric cancer; LASSO, Least Absolute Shrinkage and Selection Operator; TCGA-STAD, The Cancer Genome Atlas Stomach Adenocarcinoma; HR, hazard ratio; TPM, transcripts per million.

    Article Snippet: For gene knockdown experiments, cells were transfected with a GV493 short hairpin RNA (sh) plasmid targeting UPK1B ( ) or a negative control scrambled plasmid (sh-NC), both obtained from GeneChem, Inc.

    Techniques: Generated, Sequencing, Expressing, Selection

    UPK1B drives GC cell invasion and migration in a PI3K/AKT-dependent manner. (A) Gene set enrichment analysis indicated that genes upregulated in the UPK1B-high group were enriched in the PI3K/AKT pathway. (B) Protein levels of UPK1B in GC cell lines. (C) Knockdown of UPK1B reduced PI3K/AKT activation in MKN45 cells. Silencing UPK1B suppressed the (D) migration/invasion capacity and (E) wound closure rate of MKN45 cells. (F) Overexpression of UPK1B enhanced PI3K/AKT pathway activation in AGS cells, which was attenuated by the PI3K inhibitor LY294002. Inhibition of PI3K/AKT signaling reversed UPK1B-induced (G) migration/invasion capacity and (H) wound closure rate of AGS cells. UPK1B, uroplakin 1B; GC, gastric cancer; p-, phosphorylated; sh, short hairpin RNA; NC, negative control; OE, overexpression.

    Journal: Experimental and Therapeutic Medicine

    Article Title: CDX2-UPK1B-PIK3IP1-PI3K/AKT signaling axis regulates gastric cancer cell invasion and migration and influences patient prognosis

    doi: 10.3892/etm.2026.13179

    Figure Lengend Snippet: UPK1B drives GC cell invasion and migration in a PI3K/AKT-dependent manner. (A) Gene set enrichment analysis indicated that genes upregulated in the UPK1B-high group were enriched in the PI3K/AKT pathway. (B) Protein levels of UPK1B in GC cell lines. (C) Knockdown of UPK1B reduced PI3K/AKT activation in MKN45 cells. Silencing UPK1B suppressed the (D) migration/invasion capacity and (E) wound closure rate of MKN45 cells. (F) Overexpression of UPK1B enhanced PI3K/AKT pathway activation in AGS cells, which was attenuated by the PI3K inhibitor LY294002. Inhibition of PI3K/AKT signaling reversed UPK1B-induced (G) migration/invasion capacity and (H) wound closure rate of AGS cells. UPK1B, uroplakin 1B; GC, gastric cancer; p-, phosphorylated; sh, short hairpin RNA; NC, negative control; OE, overexpression.

    Article Snippet: For gene knockdown experiments, cells were transfected with a GV493 short hairpin RNA (sh) plasmid targeting UPK1B ( ) or a negative control scrambled plasmid (sh-NC), both obtained from GeneChem, Inc.

    Techniques: Migration, Knockdown, Activation Assay, Over Expression, Inhibition, shRNA, Negative Control

    CDX2 acts as a transcriptional repressor of UPK1B and its high expression is associated with favorable prognosis of patients with GC. (A) Venn diagram showing overlapping predicted transcriptional regulators of UPK1B from ChEA and ChEA3 databases. (B) Knockdown of CDX2 in AGS cells resulted in increased UPK1B (C) mRNA and (D) protein expression. (E) Overexpression of CDX2 in MKN45 cells reduced UPK1B protein levels. Data from (F) The Cancer Genome Atlas Stomach Adenocarcinoma cohort and (G) the Kaplan-Meier plotter database indicated that high CDX2 expression was associated with improved prognosis of patients with GC. UPK1B, uroplakin 1B; GC, gastric cancer; si, small interfering RNA; NC, negative control; OE, overexpression; HR, hazard ratio; CDX2, caudal-related homeobox transcription factor 2; ChEA, ChIP-X Enrichment Analysis.

    Journal: Experimental and Therapeutic Medicine

    Article Title: CDX2-UPK1B-PIK3IP1-PI3K/AKT signaling axis regulates gastric cancer cell invasion and migration and influences patient prognosis

    doi: 10.3892/etm.2026.13179

    Figure Lengend Snippet: CDX2 acts as a transcriptional repressor of UPK1B and its high expression is associated with favorable prognosis of patients with GC. (A) Venn diagram showing overlapping predicted transcriptional regulators of UPK1B from ChEA and ChEA3 databases. (B) Knockdown of CDX2 in AGS cells resulted in increased UPK1B (C) mRNA and (D) protein expression. (E) Overexpression of CDX2 in MKN45 cells reduced UPK1B protein levels. Data from (F) The Cancer Genome Atlas Stomach Adenocarcinoma cohort and (G) the Kaplan-Meier plotter database indicated that high CDX2 expression was associated with improved prognosis of patients with GC. UPK1B, uroplakin 1B; GC, gastric cancer; si, small interfering RNA; NC, negative control; OE, overexpression; HR, hazard ratio; CDX2, caudal-related homeobox transcription factor 2; ChEA, ChIP-X Enrichment Analysis.

    Article Snippet: For gene knockdown experiments, cells were transfected with a GV493 short hairpin RNA (sh) plasmid targeting UPK1B ( ) or a negative control scrambled plasmid (sh-NC), both obtained from GeneChem, Inc.

    Techniques: Expressing, Knockdown, Over Expression, Small Interfering RNA, Negative Control

    UPK1B activates PI3K/AKT signaling by antagonizing the inhibitory regulator PIK3IP1 in gastric cancer cells. (A) Venn diagram showing that PIK3IP1 was identified as a putative UPK1B-interacting partner based on BioGRID and HIPPIE protein-protein interaction databases. (B) UPK1B and PIK3IP1 co-localized in the cytoplasm and plasma membrane of MKN45 cells. (C) Interaction between UPK1B and PIK3IP1 in MKN45 cells. (D) Knockdown of PIK3IP1 in MKN45 cells. (E) Silencing PIK3IP1 in UPK1B-knockdown MKN45 cells restored PI3K/AKT pathway activation. Knockdown of PIK3IP1 reversed the decrease in (F) migration/invasion and (G) wound-healing capacity in UPK1B-silenced MKN45 cells. UPK1B, uroplakin 1B; p-, phosphorylated; si, small interfering RNA; sh, short hairpin RNA; NC, negative control; PIK3IP1, PI3K inhibitor interacting protein 1; HIPPIE, Human Integrated Protein-Protein Interaction Reference; IP, immunoprecipitation.

    Journal: Experimental and Therapeutic Medicine

    Article Title: CDX2-UPK1B-PIK3IP1-PI3K/AKT signaling axis regulates gastric cancer cell invasion and migration and influences patient prognosis

    doi: 10.3892/etm.2026.13179

    Figure Lengend Snippet: UPK1B activates PI3K/AKT signaling by antagonizing the inhibitory regulator PIK3IP1 in gastric cancer cells. (A) Venn diagram showing that PIK3IP1 was identified as a putative UPK1B-interacting partner based on BioGRID and HIPPIE protein-protein interaction databases. (B) UPK1B and PIK3IP1 co-localized in the cytoplasm and plasma membrane of MKN45 cells. (C) Interaction between UPK1B and PIK3IP1 in MKN45 cells. (D) Knockdown of PIK3IP1 in MKN45 cells. (E) Silencing PIK3IP1 in UPK1B-knockdown MKN45 cells restored PI3K/AKT pathway activation. Knockdown of PIK3IP1 reversed the decrease in (F) migration/invasion and (G) wound-healing capacity in UPK1B-silenced MKN45 cells. UPK1B, uroplakin 1B; p-, phosphorylated; si, small interfering RNA; sh, short hairpin RNA; NC, negative control; PIK3IP1, PI3K inhibitor interacting protein 1; HIPPIE, Human Integrated Protein-Protein Interaction Reference; IP, immunoprecipitation.

    Article Snippet: For gene knockdown experiments, cells were transfected with a GV493 short hairpin RNA (sh) plasmid targeting UPK1B ( ) or a negative control scrambled plasmid (sh-NC), both obtained from GeneChem, Inc.

    Techniques: Clinical Proteomics, Membrane, Knockdown, Activation Assay, Migration, Small Interfering RNA, shRNA, Negative Control, Immunoprecipitation