ArticleOncogene2015
Angiomotin decreases lung cancer progression by sequestering oncogenic YAP/TAZ and decreasing Cyr61 expression.
Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed.
- AMOT mediates YAP1 activation and promotes the cell progression and glycolysis in non-small cell lung cancer by modulating the Hippo signaling pathway.Translational cancer research · 2026Article
- Preferential Upregulation of AMOT-p80 Is Associated with YAP-Linked Resistance to 5-Fluorouracil and Oxaliplatin in Colorectal Cancer Cells.Biomolecules · 2026Article
- Basroparib inhibits YAP-driven cancers by stabilizing angiomotin.Molecular oncology · 2026Article
- Review
- PSAT1 promotes the progression of colorectal cancer by regulating Hippo-YAP/TAZ-ID1 axis via AMOT.Molecular and cellular biochemistry · 2025Article
- Dietary Palmitic Acid Drives a Palmitoyltransferase ZDHHC15-YAP Feedback Loop Promoting Tumor Metastasis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Association of low angiomotin-p130 and high YAP1 nuclear expression with adverse prognosis in epithelial ovarian cancer.Histology and histopathology · 2025Article
- Unraveling the Hippo pathway: YAP/TAZ as central players in cancer metastasis and drug resistance.EXCLI journal · 2025Review
- The roles of periostin derived from cancer-associated fibroblasts in tumor progression and treatment response.Cancer metastasis reviews · 2024Review
- The Hippo Pathway in Breast Cancer: The Extracellular Matrix and Hypoxia.International journal of molecular sciences · 2024Review
- Role of angiomotin family members in human diseases (Review).Experimental and therapeutic medicine · 2024Review
- YAP1-CPNE3 positive feedback pathway promotes gastric cancer cell progression.Cellular and molecular life sciences : CMLS · 2024Article
- ACADL-YAP axis activity in non-small cell lung cancer carcinogenicity.Cancer cell international · 2024Article
- Targeting the YAP/TAZ Hippo signaling pathway for oral cancer treatment.EXCLI journal · 2024Article
- Determining the minimal amount of DMSO necessary to stabilize the Angiomotin lipid binding domain.Indiana University journal of undergraduate research · 2024Article
- Factor-inhibiting HIF (FIH) promotes lung cancer progression.JCI insight · 2023Article
- Review
- Soluble CD146, a biomarker and a target for preventing resistance to anti-angiogenic therapy in glioblastoma.Acta neuropathologica communications · 2022Article
- MPDZ as a novel epigenetic silenced tumor suppressor inhibits growth and progression of lung cancer through the Hippo-YAP pathway.Oncogene · 2021Article
- Angiomotin-p130 inhibits vasculogenic mimicry formation of small cell lung cancer independently of Smad2/3 signal pathway.Journal of bioenergetics and biomembranes · 2021Article
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung cancer is the leading cause of cancer death worldwide, with metastasis underlying majority of related deaths. Angiomotin (AMOT), a scaffold protein, has been shown to interact with oncogenic Yes-associated protein/transcriptional co-activator with a PDZ-binding motif (YAP/TAZ) proteins, suggesting a potential role in tumor progression. However, the functional role of AMOT in lung cancer remains unknown. This study aimed to identify the patho-physiological characteristics of AMOT in lung cancer progression. Results revealed that AMOT expression was significantly decreased in clinical lung cancer specimens. Knockdown of AMOT in a low metastatic CL1-0 lung cancer cell line initiated cancer proliferation, migration, invasion and epithelial-mesenchymal transition. The trigger of cancer progression caused by AMOT loss was transduced by decreased cytoplasmic sequestration and increased nuclear translocation of oncogenic co-activators YAP/TAZ, leading to increased expression of the growth factor, Cyr61. Tumor promotion by AMOT knockdown was reversed when YAP/TAZ or Cyr61 was absent. Further, AMOT knockdown increased the growth and spread of Lewis lung carcinoma in vivo. These findings suggest that AMOT is a crucial suppressor of lung cancer metastasis and highlight its critical role as a tumor suppressor and its potential as a prognostic biomarker and therapeutic target for lung cancer.
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