ArticleOncogene2020
SASH1 suppresses triple-negative breast cancer cell invasion through YAP-ARHGAP42-actin axis.
Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- Focal Adhesion Kinase (FAK)-Hippo/YAP transduction signaling mediates the stimulatory effects exerted by S100A8/A9-RAGE system in triple-negative breast cancer (TNBC).Journal of experimental & clinical cancer research : CR · 2022Pooled it
- SASH1 Inhibits Gastric Cancer Progression by Regulating YAP1-Mediated Metabolic Reprogramming.Applied biochemistry and biotechnology · 2026Article
- DNA Hypomethylation ofInternational journal of molecular sciences · 2026Article
- Computational Phosphosite-Specific Network Analysis of YES1 Y426 Reveals Cancer-Associated Phosphorylation Patterns.Proteomes · 2026Article
- Combined Transcriptomic and Proteomic Forecast Analyses for Potential Biomarkers of Smoking-Induced Benign and Malignant Transformation of Vocal Fold Lesions.World journal of otorhinolaryngology - head and neck surgery · 2026Article
- Tight Spaces, Big Discoveries: Decoding Human Adhesion Biology with Avian Chorioallantoic Membrane Xenograft Models.Cancers · 2026Review
- SPTLC2 drives an EGFR-FAK-HBEGF signaling axis to promote ovarian cancer progression.Oncogene · 2025Article
- FAM49B suppresses ovarian cancer cell growth through regulating MAPK signaling.American journal of cancer research · 2025Article
- Review
- Low temperature plasma suppresses proliferation, invasion, migration and survival of SK-BR-3 breast cancer cells.Molecular biology reports · 2023Article
- UM-164, a Dual Inhibitor of c-Src and p38 MAPK, Suppresses Proliferation of Glioma by Reducing YAP Activity.Cancers · 2022Article
- GRHL2 Enhances Phosphorylated Estrogen Receptor (ER) Chromatin Binding and Regulates ER-Mediated Transcriptional Activation and Repression.Molecular and cellular biology · 2022Article
- SUFU suppresses ferroptosis sensitivity in breast cancer cells via Hippo/YAP pathway.iScience · 2022Article
- The biology of YAP in programmed cell death.Biomarker research · 2022Review
- The 3D in vivo chorioallantoic membrane model and its role in breast cancer research.Journal of cancer research and clinical oncology · 2022Review
- HJURP regulates cell proliferation and chemo-resistance via YAP1/NDRG1 transcriptional axis in triple-negative breast cancer.Cell death & disease · 2022Article
- Pan-Cancer Integrated Analysis Identification of SASH3, a Potential Biomarker That Inhibits Lung Adenocarcinoma Progression.Frontiers in oncology · 2022Article
- Long Noncoding-RNA Component of Mitochondrial RNA Processing Endoribonuclease Promotes Carcinogenesis in Triple-Negative Breast Cancer Cells via the Competing Endogenous RNA Mechanism.Journal of breast cancer · 2021Article
- A homozygous stop-gain variant in ARHGAP42 is associated with childhood interstitial lung disease, systemic hypertension, and immunological findings.PLoS genetics · 2021Article
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triple-negative breast cancer (TNBC) is extremely aggressive and lacks effective therapy. SAM and SH3 domain containing1 (SASH1) has been implicated in TNBC as a candidate tumor suppressor; however, the mechanisms of action of SASH1 in TNBC remain underexplored. Here, we show that SASH1 was significantly downregulated in TNBC patients samples compared with other subtypes of breast cancer. Ectopic SASH1 expression inhibited, while depletion of SASH1 enhanced, the invasive phenotype of TNBC cells, accompanied by deregulated expression of MMP2 and MMP9. The functional effects of SASH1 depletion were confirmed in the chicken chorioallantoic membrane and mouse xenograft models. Mechanistically, SASH1 knockdown downregulated the phosphorylation levels of the Hippo kinase LATS1 and its effector YAP (Yes associated protein), thereby upregulating YAP accumulation together with its downstream target CYR61. Consistently, forced SASH1 expression exhibited opposite effects. Pharmacological inhibition of YAP or knockdown of YAP reversed the enhanced cell invasion of TNBC cells following SASH1 depletion. Furthermore, SASH1-induced YAP signaling was LATS1-dependent, which in reverse enhanced phosphorylation of SASH1. The SASH1 S407A mutant (phosphorylation deficient) failed to rescue the altered YAP signaling by SASH1 knockdown. Notably, SASH1 depletion upregulated ARHGAP42 levels via YAP-TEAD and the YAP-ARHGAP42-actin axis contributed to SASH1-regulated TNBC cell invasion. Therefore, our findings uncover a new mechanism for the tumor-suppressive activity of SASH1 in TNBC, which may serve as a novel target for therapeutic intervention.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.