Journal: BMC oral health

Article Title: Coexpression network analysis identified MT3 as a hub gene that promotes the chemoresistance of oral cancer by regulating the expression of YAP1.

doi: 10.1186/s12903-023-03600-z

Figure Lengend Snippet: Fig. 5 MT3 promotes cisplatin resistance by modulating YAP activation in OSCC. (A-B) Western blotting showed that YAP1 expression was decreased after MT3 knockdown, while the expression of MT3 was not changed after YAP1 knockdown in CAL27-CISR or Fadu-CISR cells. (C-D) Immunohistochemical staining of YAP1 in chemotherapy-resistant OSCC tissue (CR) and chemotherapy-sensitive tissue (CS). p < 0.01**. (E) qRT‒PCR results showing YAP1 mRNA levels in CAL27-CISR or Fadu-CISR cells. (F) qRT‒PCR results showing downstream target genes of YAP1, BIRC2, CNNT1, and CTGF mRNA levels in CAL27- CISR cells. (G) BIRC2, CNNT1, and CTGF mRNA levels in Fadu-CISR cells. n = 3, p < 0.01**

Article Snippet: Fadu and CAL27 oral cancer cell lines were transfected with sgRNA against MT3 or YAP1 cloned in PX459 (Addgene, USA).

Techniques: Activation Assay, Western Blot, Expressing, Knockdown, Immunohistochemical staining, Staining

Journal: BMC oral health

Article Title: Coexpression network analysis identified MT3 as a hub gene that promotes the chemoresistance of oral cancer by regulating the expression of YAP1.

doi: 10.1186/s12903-023-03600-z

Figure Lengend Snippet: Fig. 6 YAP1 inhibition suppresses the development of CIS resistance. (A) Cell survival declined after verteporfin (VP) treatment in CAL27-CISR or Fadu- CISR cells. (B) Cell proliferation was suppressed after VP treatment in CAL27-CISR or Fadu-CISR cells for 24 h, 48 and 72 h. (C) Compared with the DMSO group, the number of colonies was reduced after VP treatment in CAL27-CISR or Fadu-CISR cells. The results are presented as the mean ± SEM of three independent experiments. (D-G) CAL27-CISR or Fadu-CISR cells were subcutaneously inoculated into nude mice (n = 6) and then treated with DMSO (negative control), cisplatin, verteporfin, or cisplatin combined with verteporfin. Tumor growth (D, F) and survival analysis (E, G) were determined as indicated. (p < 0.05*, p < 0.01**, p < 0.001***)

Article Snippet: Fadu and CAL27 oral cancer cell lines were transfected with sgRNA against MT3 or YAP1 cloned in PX459 (Addgene, USA).

Techniques: Inhibition, Negative Control

Journal: Scientific Reports

Article Title: Blocking YAP1–Liprin-β2 interaction impedes metastasis and promotes tumor suppression in head and neck squamous carcinoma

doi: 10.1038/s41598-025-11652-0

Figure Lengend Snippet: YAP1 is crucial for invasion and migration in YAP1 activated HNSCC cell lines. ( A ) YAP1-associated gene signature subtypes in HNSCC cell lines (n = 17 in CCLE data set). HNSCC cell lines were stratified according to Support vector machine (SVM) predictor probability from the YAP1 predictor. Blue indicates YAP1 inactivation (YI) and orange indicates YAP1 activation (YA). The cell lines highlighted in asterisk in the table represent the cell lines used in subsequent experiments. ( B ) YAP1 protein expression of 17 HNSCC cells are shown using western blot (WB). β-actin was loaded as a control. ( C ) Knockdown of YAP1 using siRNA was determined to decrease the band in WB results in SNU1041 and SCC9 cell lines. ( D ) Representative images of the cell invasion ability assay are shown. The effects of different treatments on the invasion ability of SNU1041 and SCC9 cells were determined by counting the number of invading cells. Data are means ± SEM. (n = 3). Statistical significance was determined using a t-test. *** p < 0.005 versus control. SEM, standard error of the mean. ( E ) Representative images of migration assays were shown in SNU1041 and SCC9 cell lines. The quantitative graph represents the percentage of wounded area. The microscopical images were acquired after 48 h of both cells were scratched. ( F ) SCC25 cells were transfected with GFP-conjugated empty and YAP1 vectors. YAP1 protein expression was evaluated through WB in transfected cells. ( G ) Representative images of invaded cells were acquired by invasion ability assay. The quantitative graph shows the number of invading cells. ( H ) Representative images of migration assays were shown in SCC25 cell line. ( I ) Protein level of EMT markers were evaluated with treatment of siGFP and siYAP1. ( J ) EMT markers were evaluated with empty and YAP1 vectors using WB. GAPDH was loaded as a control.

Article Snippet: pCMV-YAP1 plasmid containing the coding region of the human YAP1 gene ( NM_001130145 ) was purchased from Addgene (#66853).

Techniques: Migration, Plasmid Preparation, Activation Assay, Expressing, Western Blot, Control, Knockdown, Transfection

Journal: Scientific Reports

Article Title: Blocking YAP1–Liprin-β2 interaction impedes metastasis and promotes tumor suppression in head and neck squamous carcinoma

doi: 10.1038/s41598-025-11652-0

Figure Lengend Snippet: YAP1-mediated negative regulation of PPFIBP2/Liprin-β2 is crucial role in invasion and maigration of HNSCC. ( A ) Venn diagram showing the relationship between 77 genes with significance in the recurrence-free survival rate of HNSCC patients and the top 1000 of YAP1-bound genes with 1 kb from TSS derived from chip-atlas. It shows the overlap three candidates of invasion or metastasis involved sub-factor of YAP1. MACS; Model-based Analysis of ChIP-seq algorithm. ( B ) The correlation plot between YAP1 and PPFIBP2/Liprin-β2 gene. The correlation coefficient value was calculated using Pearson’s correlation method (r = − 0.14 and p = 0.002). ( C ) SNU1041 and SCC9 cells were treated with siYAP1, the mRNA level of PPFIBP2/Liprin-b2 was evaluated using qRT-PCR. ( D ) The protein level of PPFIBP2/Liprin-b2 was evaluated in SNU1041 and SCC9 cells treated with siYAP1. ( E ) Representative images of the cell invasion ability assay were shown. The effects of different treatments on the invasion ability of SNU1041 and SCC9 cells were determined by counting the number of invading cells. Data are means ± SEM. (n = 3). Statistical significance was determined using a t-test. *** p < 0.005 versus control. SEM, standard error of the mean. ( F ) Representative images of migration assays were shown in SNU1041 and SCC9 cell lines with treatment of siYAP1 or siYAP1 + siPPFIBP2. The quantitative graph represents the percentage of wounded area. The microscopical images were acquired after 48 h of both cells were scratched. ( G ) The protein levels of EMT markers were evaluated with treatment of siYAP1 or siYAP1 + siPPFIBP2 in SNU1041 and SCC9 cell lines. ( H ) YAP1 suppresses the expression of PPFIBP2/Liprin-β2 to regulate EMT markers, resulting in increased invasion and migration, which leads to a poor prognosis in HNSCC cells. The YAP1 inhibitor CA3 inhibits this YAP1-PPFIBP2 axis, reducing invasion and migration in HNSCC cells, thereby potentially improving prognosis.

Article Snippet: pCMV-YAP1 plasmid containing the coding region of the human YAP1 gene ( NM_001130145 ) was purchased from Addgene (#66853).

Techniques: Derivative Assay, ChIP-sequencing, Quantitative RT-PCR, Control, Migration, Expressing

Journal: Scientific Reports

Article Title: Blocking YAP1–Liprin-β2 interaction impedes metastasis and promotes tumor suppression in head and neck squamous carcinoma

doi: 10.1038/s41598-025-11652-0

Figure Lengend Snippet: The reverse axis of YAP1-PPFIBP2 is strongly correlated with LN metastasis and survival in patients with HNSCC. ( A ) A box plot was used to compare the expression levels of YAP1 and PPFIBP2 mRNA between group YA and group YI. Significance was calculated by a two-tailed t-test. ( B ) A box plot was used to compare the percentages of pathological N stages based on PPFIBP2 expression levels between Group YA and Group YI. ( C ) The Kaplan–Meier plot illustrates the differences in overall survival (OS) between two groups: YA with low PPFIBP2 expression (PPFIBP2-L) and YI with high PPFIBP2 expression (PPFIBP2-H).

Article Snippet: pCMV-YAP1 plasmid containing the coding region of the human YAP1 gene ( NM_001130145 ) was purchased from Addgene (#66853).

Techniques: Expressing, Two Tailed Test

Journal: Scientific Reports

Article Title: Blocking YAP1–Liprin-β2 interaction impedes metastasis and promotes tumor suppression in head and neck squamous carcinoma

doi: 10.1038/s41598-025-11652-0

Figure Lengend Snippet: The YAP1 inhibitor, CA3 controls EMT markers and reduces cell invasion and migration. ( A ) The representative figure displays the comparative invasion abilities between the non-treated group and the CA3-treated group. Accompanying this, a quantitative graph presents the counting numbers of invaded cells, providing a numerical representation of the invasion assays. ( B ) HNSCC cells were treated with 0.5 µM of CA3. The expression levels of EMT marker proteins between non-treated and CA3-treated groups were compared using Western blot analysis. ( C ) Representative images depict the results of the migration assays on cells. The quantitative graph shows the percentage of the wounded area 48 h post-treatment with CA3. The significance of the differences observed was calculated using a t-test, with a highly significant result indicated by *** p < 0.005.

Article Snippet: pCMV-YAP1 plasmid containing the coding region of the human YAP1 gene ( NM_001130145 ) was purchased from Addgene (#66853).

Techniques: Migration, Expressing, Marker, Western Blot

Journal: Materials Today Bio

Article Title: Age-mimicking hydrogel stiffness recapitulates the mechanical niche of the hippocampus to regulate neural stem cell senescence

doi: 10.1016/j.mtbio.2026.102985

Figure Lengend Snippet: Age-associated hippocampal stiffening and its replication via laminin-modified hydrogels . (a) The strategy of in vivo EdU labeling and marker immunostaining for analyzing NSC proliferation and neurogenesis across various mouse age groups. ( b ) Co-staining of GFAP, EdU, and DCX in the hippocampus across different ages. Representative images showing a reduction in active radial glia-like stem cells and neuroblasts/newborn neurons with increasing age. GFAP (green), DCX (red), EdU (gray), and DAPI (blue). Scale bar, 100 μm. ( c-e ) Quantification of active radial glia-like stem cells (GFAP + EdU + ) ( c ), neuroblasts (DCX + EdU + ) ( d ), and newborn neurons (DCX + ) (e) in the SGZ area as in ( b ). n = 3 or 4 mice per group. ( f ) Schematic showing the measurement of hippocampal tissue stiffness using the Pavone nanoindenter and the design of hyaluronic acid (HA)–laminin hydrogels with tunable stiffness to mimic hippocampal mechanical properties at different postnatal ages. Soft, medium, and stiff hydrogels correspond to the mechanical characteristics of hippocampal tissues from 1-, 4-, and 12-week-old mice, respectively. ( g ) Representative images of the dentate gyrus in mouse brain slices across age groups, captured under Pavone nanoindentation microscopy. The SGZ regions measured by the nanoindentation probe are demarcated by paired colorful dashed lines. ( h ) Quantification of Young’s modulus in the hippocampal SGZ region of mice at different ages using Pavone nanoindentation. Brain slices were obtained from four mice per age group. Measurements were taken from n = 227 spots (1 week), n = 149 spots (4 weeks), n = 241 spots (8 weeks), n = 157 spots (12 weeks). (i ) Schematic illustration of the synthesis of HA@HA and HA@HA–Laminin hydrogels. Hyaluronic acid (HA) was first crosslinked with adipic dihydrazide (ADH) using EDC/HCl activation under acidic conditions (pH 3–4) to form HA@HA. Subsequently, laminin was conjugated to the HA network via CDI-mediated coupling to generate HA@HA–Laminin hydrogels. ( j ) Quantification of Young’s modulus of Soft, Medium, and Stiff HA-laminin hydrogels using the same Pavone nanoindentation used for tissue (Soft hydrogel, n = 44 spots; Medium hydrogel, n = 37 spots; Stiff hydrogel, n = 29 spots). ( k ) Immunostaining of YAP1 protein shows the subcellular localization of YAP1 in NSCs cultured on HA-laminin hydrogels of varying stiffness. Dashed lines indicate representative cells with YAP1 predominantly in the cytoplasm (indicated by arrowheads), while solid lines represent cells with YAP1 primarily in the nucleus (indicated by arrows). Scale bar, 20 μm. ( l ) Quantification of YAP1 distribution in NSCs as in ( k ) (n = 4 wells). For all quantification data, statistical significance was determined using one-way ANOVA with Tukey’s multiple comparison tests. Data are presented as mean ± SD (∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001).

Article Snippet: The sections were incubated overnight at 4 °C with primary antibodies: GFAP (Sigma, AB5541, 1:1000), GFAP (Invitrogen, 13-0300, 1:1000) Doublecortin (Abcam, AB18723, 1:500) and Yap1 (Proteintech, 13584-1-AP, 1:800).

Techniques: Modification, In Vivo, Labeling, Marker, Immunostaining, Staining, Microscopy, Activation Assay, Cell Culture, Comparison

Journal: Developmental cell

Article Title: Flow-Dependent Endothelial YAP Regulation Contributes to Vessel Maintenance.

doi: 10.1016/j.devcel.2017.02.019

Figure Lengend Snippet: Figure 2. Yap1/TEAD-Dependent Transcription Becomes Active in Perfused Vessels (A) The constructs used to monitor Yap1 responses in EC by using fli1 promoter (EC-specific TEAD reporter). (B) Projection view of confocal stack fluorescence images of the trunk region in Tg(fli1:Gal4db-TEAD2DN-2A-mC);(UAS:GFP);(fli1:Myr-mC) WT (left) and ho- mozygous yap1ncv101 mutant embryos (right) at 50 hpf. Lateral views, anterior to the left. Upper panels, GFP images (green); lower panels, merged images (GFP, green; Myr-mC, red). White arrows indicate GFP signal-positive ECs of lumenized blood vessels. Representative images of four independent experiments are shown. (C) Projection view of confocal images of the trunk region in Tg(fli1:Gal4db-TEAD2DN-2A-mC);(UAS:GFP);(fli1:Myr-mC) embryos (at 32 and 50 hpf as indicated at the left) injected with Qdot 655 (white) into the heart to visualize perfused vessels. Left, GFP images (green); right, merged images (Qdot 655, white; GFP, green; Myr-mC, red). While a significant population of ECs of perfused vessels expresses GFP (white arrows), ECs of non-perfused vessels do not (magenta arrows). (D) Projection view of confocal images of the trunk region of fixed Tg(fli1:EGFP-YAP) embryos (at 27–50 hpf as indicated at the top) immunostained with anti-GFP antibody (green) together with DAPI (blue). White and orange arrowheads indicate EGFP-YAP in the cytoplasm and nucleus, respectively. (E) Graph shows percentage of the number of the ECs in which EGFP-YAP is excluded from the nucleus (N < C, white bars) and those in which EGFP-YAP is localized in the nucleus (N > C or N = C, black bars) at the indicated stages of the dorsal aorta (DA) and the arterial intersomitic vessels (aISVs) among the total number of observed ECs (indicated at the top) from 7 to 10 embryos. (F) Time-sequential two-photon images of ISVs in Tg(fli1:EGFP-YAP) embryos that were about to form lumen (from 37 hpf). Elapsed time (min) is indicated at the left. Yellow asterisks indicate newly formed lumens connecting to the circulation. White and orange arrowheads indicate EGFP-YAP in the cytoplasm and nucleus, respectively. Representative images of seven independent experiments are shown. Scale bars, 10 mm. See also Figure S2.

Article Snippet: After removing chorionic membrane and yolk sac, wild-type or homozygous yap1ncv101 mutant embryos were directly lysed in 1 x SDS sample buffer and subjected toWestern blot analysis with a rabbit anti-YAP antibody (Novus Biologicals) recognizing zebrafish Yap1 and with an anti-b-actin antibody.

Techniques: Construct, Mutagenesis, Injection

Journal: Developmental cell

Article Title: YAP Partially Reprograms Chromatin Accessibility to Directly Induce Adult Cardiogenesis in Vivo

doi: 10.1016/j.devcel.2019.01.017

Figure Lengend Snippet: KEY RESOURCES TABLE

Article Snippet: Rabbit YAP1 antibody , Novus biologicals , Cat#NB110-583538.

Techniques: Virus, Plasmid Preparation, Recombinant, Imaging, SYBR Green Assay, Gene Expression, Control, Software, Next-Generation Sequencing