ArticleLife science alliance2018
LATS1 and LATS2 suppress breast cancer progression by maintaining cell identity and metabolic state.
Article in Life science alliance, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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
21 citing papers in PubMed, 33 citations in OpenAlex.
- LATS kinase activity and tumor suppressor function are regulated by a second autophosphorylation site.The Journal of biological chemistry · 2026Article
- LATS2 expression differences in lung adenocarcinoma and lung squamous cell carcinoma analyzed using bioinformatics and experimental approaches.Oncology letters · 2026Article
- YAP1 Dysfunction Promotes Molecular Properties Linked to Breast Cancer Susceptibility.Cancer prevention research (Philadelphia, Pa.) · 2026Article
- Hippo signaling pathway in cervical cancer: insights into mechanisms and therapeutic potential.Frontiers in oncology · 2025Review
- Breast cancer genomic analyses reveal genes, mutations, and signaling networks.Functional & integrative genomics · 2024Article
- New Insights into YAP/TAZ-TEAD-Mediated Gene Regulation and Biological Processes in Cancer.Cancers · 2023Review
- Inflammatory signaling pathways in the treatment of Alzheimer's disease with inhibitors, natural products and metabolites (Review).International journal of molecular medicine · 2023Review
- Mechanisms underlying divergent relationships between CaThe Journal of physiology · 2023Article
- Inactivation of LATS1/2 drives luminal-basal plasticity to initiate basal-like mammary carcinomas.Nature communications · 2022Article
- Article
- Pathological significance and prognostic role of LATS2 in prostate cancer.The Prostate · 2021Article
- lncRNA TINCR attenuates the proliferation and invasion, and enhances the apoptosis of cutaneous malignant melanoma cells by regulating the miR‑424‑5p/LATS1 axis.Oncology reports · 2021Article
- Identification of the tumor‑suppressive role of circular RNA‑FOXO3 in colorectal cancer via regulation of miR‑543/LATS1 axis.Oncology reports · 2021Article
- Article
- Circular RNA circ_103820 suppresses lung cancer tumorigenesis by sponging miR-200b-3p to release LATS2 and SOCS6.Cell death & disease · 2021Article
- A Division of Labor between YAP and TAZ in Non-Small Cell Lung Cancer.Cancer research · 2020Article
- Expression of large tumour suppressor (LATS) kinases modulates chemotherapy response in advanced non-small cell lung cancer.Translational lung cancer research · 2020Article
- MiR-429 Involves in the Pathogenesis of Colorectal Cancer via Directly Targeting LATS2.Oxidative medicine and cellular longevity · 2020Article
- The spectraplakin Dystonin antagonizes YAP activity and suppresses tumourigenesis.Scientific reports · 2019Article
- The Hippo Pathway in Prostate Cancer.Cells · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 3 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deregulated activity of LArge Tumor Suppressor (LATS) tumor suppressors has broad implications on cellular and tissue homeostasis. We examined the consequences of down-regulation of either LATS1 or LATS2 in breast cancer. Consistent with their proposed tumor suppressive roles, expression of both paralogs was significantly down-regulated in human breast cancer, and loss of either paralog accelerated mammary tumorigenesis in mice. However, each paralog had a distinct impact on breast cancer. Thus, LATS2 depletion in luminal B tumors resulted in metabolic rewiring, with increased glycolysis and reduced peroxisome proliferator-activated receptor γ (PPARγ) signaling. Furthermore, pharmacological activation of PPARγ elicited LATS2-dependent death in luminal B-derived cells. In contrast, LATS1 depletion augmented cancer cell plasticity, skewing luminal B tumors towards increased expression of basal-like features, in association with increased resistance to hormone therapy. Hence, these two closely related paralogs play distinct roles in protection against breast cancer; tumors with reduced expression of either LATS1 or LATS2 may rewire signaling networks differently and thus respond differently to anticancer treatments.
Identifiers
What OpenQuestion holds
Registered trials
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.