Journal: Journal of Traditional and Complementary Medicine

Article Title: Bushen Huoxue Recipe enhances the immune microenvironment at the maternal-fetal interface via the Hippo signaling pathway in mice with recurrent spontaneous abortion

doi: 10.1016/j.jtcme.2025.02.005

Figure Lengend Snippet: Effect of BSHXR on the Hippo signaling pathway. (A) The expression levels of proteins in the Hippo pathway. (B) Quantification of the protein levels. (p-MST/t-MST: Con vs. RSA, p = 0.0179; RSA vs. CsA, p = 0.8320; RSA vs. BSHXR, p = 0.0450; p-LATS/t-LATS: Con vs. RSA, p = 0.0030; RSA vs. CsA, p = 0.0153; RSA vs. BSHXR, p = 0.0327; p-YAP/t-YAP: Con vs. RSA, p = 0.0131; RSA vs. CsA, p = 0.0432; RSA vs. BSHXR, p = 0.0340; p-TAZ/t-TAZ: Con vs. RSA, p = 0.0045; RSA vs. CsA, p = 0.0437; RSA vs. BSHXR, p = 0.0050). (C) Representative images of immunofluorescence staining for YAP and TAZ in decidual tissues. Scale bar: 20 μm (YAP/TAZ/DCS1). (D) The expression of YAP and TAZ in the nuclear or cytoplasmic fraction. (E) Quantification of the protein levels. (YAP: Con vs. RSA, p = 0.0079; RSA vs. CsA, p = 0.0228; RSA vs. BSHXR, p = 0.0163; TAZ: Con vs. RSA, p = 0.0001; RSA vs. CsA, p = 0.0090; RSA vs. BSHXR, p = 0.0006). The data are expressed as the means ± SEMs. ∗ p < 0.05, ∗∗ p < 0.01 and ∗∗∗ p <0.001, compared with the control group; # p < 0.05, ## p < 0.01 and ### p < 0.001, compared with the RSA group.

Article Snippet: Antibodies against TLR2 (66645-1-Ig), TLR4 (66350-1-Ig), TLR7 (17232-1-AP), and GAPDH (60004-1-Ig) were purchased from Proteintech (Rosemont, IL, USA); antibodies against RORγt (ab207082) and FoxP3 (ab215206) were purchased from Abcam (Cambridge, MA, USA); Alexa Fluor 555 nm (8953) and antibodies against MST (14946), p-MST (49332), LATS (3477S), p-LATS (8654S), YAP (14074S), p-YAP (13008S), TAZ (83669S), and p-TAZ (59971S) were purchased from Cell Signaling Technology (Danvers, MA, USA); and an antibody against Lamin B (A11495) was purchased from ABclonal (Wuhan, China).

Techniques: Expressing, Immunofluorescence, Staining, Control

Journal: Signal Transduction and Targeted Therapy

Article Title: PKC-eta promotes breast cancer metastasis by regulating the Hippo–YAP signaling pathway

doi: 10.1038/s41392-026-02572-0

Figure Lengend Snippet: AKT phosphorylation of the upstream kinase cascade of the Hippo pathway is negatively regulated by PKCη. a Western blot analysis showing the activation of members of the upstream kinase cascade of the Hippo pathway, which is regulated by AKT phosphorylation, in PKCη KO TNBC cells. PKCη promotes YAP and PTEN expression, leading to dephosphorylation and inactivation of AKT. b An AKT inhibitor (MK-2206) effectively inhibits the upstream Hippo pathway phospho-cascade regulated by AKT in PKCη KO TNBC cells. c YAP-specific siRNA downregulates PTEN expression in TNBC cells in conjunction with AKT activation. d Relative mRNA expression of PTEN and PRKCH in control and MDA-MB-231 PKCη KO cells, as determined by RT‒qPCR. Knockout of PKCη in MDA-MB-231 cells resulted in a marked reduction in PTEN transcript levels compared with those in control cells. e Impact of PKCη expression on YAP transcriptional targets in TNBC cells. f Relative mRNA expression of canonical YAP target genes ( AXL, CYR61, IGFBP3 , and TEAD ) was measured via RT‒qPCR in MDA-MB-231 PKCη KO and control cells. PKCη knockout results in a significant reduction in the expression of these downstream effectors. g Schematic illustration of how YAP activity regulates PTEN expression and modulates the AKT pathway through this feedback mechanism (in the presence or absence of PKCη). Statistical significance was determined via two-way ANOVA, where * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001

Article Snippet: The antibodies used in this study were against YAP (CST, #14074), MST1 (CST, #3682), pMST1 (CST, #3681), LATS1 (CST, #3477), 14-3-3 ζ/δ (CST, #7413), pLATS1 (CST, #8654), pYAP (Ser127) (CST, #13008), pYAP (Ser109) (CST, #53749), pYAP (Ser397) (CST, #13619), pTAZ (Ser89) (CST, #75275), TAZ (CST, #83669), PTEN (CST, #9559) Lamin B1 (CST, #13435), AKT (pan) (CST, #4691), AXL (CST, #8661), Pan-TEAD (CST, #13295), CYR61 (CST, 14479), IGFBP3 (CST, #25864), HA-Tag (CST, #3724), FLAG (CST, #14793), pAKT (Ser473) (CST, #4060), and Anti-rabbit IgG (CST, # 7074).

Techniques: Phospho-proteomics, Western Blot, Activation Assay, Expressing, De-Phosphorylation Assay, Control, Knock-Out, Activity Assay

Journal: Signal Transduction and Targeted Therapy

Article Title: PKC-eta promotes breast cancer metastasis by regulating the Hippo–YAP signaling pathway

doi: 10.1038/s41392-026-02572-0

Figure Lengend Snippet: Schematic representation of the molecular mechanism of PKCη-YAP-mediated regulation of the Hippo pathway and metastasis in TNBC. CRISPR Control: In the normal state of TNBC, PKCη inhibits the Hippo pathway (Hippo-OFF), promoting S128 phosphorylation and stabilization, which leads to the nuclear import of YAP, where it regulates the transcription of several genes related to EMT, stemness, and metastasis. Additionally, YAP regulates PTEN transcription, thereby inhibiting AKT activation of the Hippo pathway through this feedback mechanism. The activation of the PKCη-YAP axis enhances migration and invasion, thereby increasing the metastatic potential and facilitating secondary spread to the lungs, liver, and brain. PKCη knockout/uPEP2 treatment: YAP and PTEN expression decreased in the absence of PKCη. Activation of the Hippo pathway (Hippo-ON) leads to increased phosphorylation and activation of AKT, MST1, and LATS1. Phosphorylation of YAP results in the recruitment of 14-3-3 proteins that mediate cytoplasmic retention or proteolytic degradation. Treatment with uPEP2 inhibits PKCη kinase activity and decreases protein expression. Thus, pharmacological treatment of TNBC with uPEP2 phenocopied the effects of PKCη KO in BC cells, reducing their metastatic potential and reversing EMT and stemness via the PKCη–YAP Hippo pathway axis (created at https://BioRender.com )

Article Snippet: The antibodies used in this study were against YAP (CST, #14074), MST1 (CST, #3682), pMST1 (CST, #3681), LATS1 (CST, #3477), 14-3-3 ζ/δ (CST, #7413), pLATS1 (CST, #8654), pYAP (Ser127) (CST, #13008), pYAP (Ser109) (CST, #53749), pYAP (Ser397) (CST, #13619), pTAZ (Ser89) (CST, #75275), TAZ (CST, #83669), PTEN (CST, #9559) Lamin B1 (CST, #13435), AKT (pan) (CST, #4691), AXL (CST, #8661), Pan-TEAD (CST, #13295), CYR61 (CST, 14479), IGFBP3 (CST, #25864), HA-Tag (CST, #3724), FLAG (CST, #14793), pAKT (Ser473) (CST, #4060), and Anti-rabbit IgG (CST, # 7074).

Techniques: CRISPR, Control, Phospho-proteomics, Activation Assay, Migration, Knock-Out, Expressing, Activity Assay