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: Cells were also transfected with small interfering RNAs (siRNAs) targeting CDX2 or PIK3IP1 , with a universal non-targeting scrambled siRNA (si-NC) as the negative control , obtained from GeneChem, Inc. For UPK1B and CDX2 overexpression, the p-TSB-CMV-UPK1B and p-TSB-CMV-CDX2 expression vectors [Shanghai Genomeditech Co., Ltd.] and the corresponding empty p-TSB-CMV vector (negative control) were used.

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

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: Cells were also transfected with small interfering RNAs (siRNAs) targeting CDX2 or PIK3IP1 , with a universal non-targeting scrambled siRNA (si-NC) as the negative control , obtained from GeneChem, Inc. For UPK1B and CDX2 overexpression, the p-TSB-CMV-UPK1B and p-TSB-CMV-CDX2 expression vectors [Shanghai Genomeditech Co., Ltd.] and the corresponding empty p-TSB-CMV vector (negative control) were used.

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

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: Cells were also transfected with small interfering RNAs (siRNAs) targeting CDX2 or PIK3IP1 , with a universal non-targeting scrambled siRNA (si-NC) as the negative control , obtained from GeneChem, Inc. For UPK1B and CDX2 overexpression, the p-TSB-CMV-UPK1B and p-TSB-CMV-CDX2 expression vectors [Shanghai Genomeditech Co., Ltd.] and the corresponding empty p-TSB-CMV vector (negative control) were used.

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

Journal: Clinical Science (London, England : 1979)

Article Title: In vivo inhibition of TDO2 in fibroids results in widespread alteration in the tumor transcriptome

doi: 10.1042/CS20260395

Figure Lengend Snippet: Effects of TDO2 silencing in primary LSMC. Cells were transfected with siTDO2 or control siRNA (siNC) for 96 h, followed by assessment of gene expression by qRT-PCR. Expression levels of TDO2, VDR, MMP11, MMP14, COL11A1, CBX4, LINC02568, LINC01310, LINC02544, LINC02182, and miR-584-5p are shown. Data represent mean ± SEM from four independent experiments ( n = 4). Statistical significance is indicated as * P <0.05 and *** P <0.01.

Article Snippet: For gene silencing experiments, primary LSMCs were transfected with 50 nM of either a non-targeting control siRNA (siNC) or siRNA targeting TDO2 (siTDO2; 5′-CUAUCACUACCUGCGAUCAACUGUG-3′) using PureFection transfection reagent (System Biosciences, Mountain View, CA, U.S.A.), according to the manufacturer’s protocol.

Techniques: Transfection, Control, Gene Expression, Quantitative RT-PCR, Expressing

Journal: Nucleic Acids Research

Article Title: In situ tracking of glycoRNAs on single-cell surface to reveal RNA heterogeneity and transport mechanism

doi: 10.1093/nar/gkag362

Figure Lengend Snippet: SNARE protein knockdown verification and colocalization analysis with glycoRNA. ( A ) Relative mRNA expression of v-SNARE protein after siRNA-mediated knockdown was determined by quantitative real-time PCR (qPCR). ( B ) Protein expression levels of v-SNARE protein were detected by Western blot. ( C ) Quantitative analysis of Western blot result( B ). ( D ) Relative mRNA expression of t-SNARE protein after siRNA-mediated knockdown was determined by quantitative real-time PCR (qPCR). ( E ) Protein expression levels of t-SNARE protein were detected by Western blot. ( F ) Quantitative analysis of Western blot result ( E ). Data are presented as mean ± SD ( n = 3). ( G ) Co-localization of t-SNARE (TSNARE1 channel) and v-SNARE (VTI1B channel) with GLINT-labeled glycoRNAs in the images (FAM channel). ( H ) The plot profiles show co-localization of glycoRNAs with t-SNARE or v-SNARE.

Article Snippet: siRNAs targeting human VTI1B, TSNARE1, and GAPDH, as well as a non-targeting negative control siRNA, were synthesized by Sangon Biotech (Shanghai, China).

Techniques: Knockdown, Expressing, Real-time Polymerase Chain Reaction, Western Blot, Labeling