Loss of DLG5 promotes breast cancer malignancy by inhibiting the Hippo signaling pathway
Open accessAbstract
Discs Large Homolog 5 (DLG5) plays an important role in the maintenance of epithelial cell polarity. Recent research showed that DLG5 is decreased in Yes-associated protein (YAP)-overexpressing cells. However, the exact relationship between DLG5 and YAP is not clear. In this study, we showed that loss of DLG5 promoted breast cancer cell proliferation by inhibiting the Hippo signaling pathway and increasing nuclear YAP expression. Furthermore, depletion of DLG5 induced epithelial-mesenchymal transition (EMT) and disrupted epithelial cell polarity, which was associated with altered expression of Scribble, ZO1, E-cadherin and N-cadherin and their mislocalization. Interestingly, we first reported that loss of DLG5 inhibited the interaction of Mst1 and Lats1 with Scribble, which was crucial for YAP activation and the transcription of TEA domain (TEAD) family members. In summary, loss of DLG5 expression promoted breast cancer malignancy by inactivating the Hippo signaling pathway and increasing nuclear YAP.
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Many Scribble binding partners localizing to adherens or tight junctions have been identified, some by coimmunoprecipitation in a complex with intact Scribble protein, and others for which the interaction is direct and maps to the PDZ domains.
“Many Scribble binding partners localizing to adherens or tight junctions have been identified, some by coimmunoprecipitation in a complex with the intact Scribble protein (e.g., ZO-1 or DLG5; Ivanov et al., 2010; Liu et al., 2017), and others for which the interaction is direct and maps to the PDZ domains (e.g., β-catenin, the Rho GAP DLC3; Ivarsson et al., 2014; Hendrick et al., 2016).”
From Scribble: A master scaffold in polarity, adhesion, synaptogenesis, and proliferation (2019) · cites this paper as Liu et al., 2017
Scribble recruitment to adherens junctions is Ecad dependent in MDCK cells and depends on DLG5 in MCF-10A cells.
“Scribble recruitment to adherens junctions is Ecad dependent in MDCK cells (Navarro et al., 2005) and depends on DLG5 in MCF-10A cells (Liu et al., 2017).”
From Scribble: A master scaffold in polarity, adhesion, synaptogenesis, and proliferation (2019) · cites this paper as Liu et al., 2017
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References 46 · Cited by 61
- Authors
- Liu, J., Li, J., Li, P., Wang, Y., Liang, Z., Jiang, Y., Li, J., Feng, C., Wang, R., Chen, H., Zhou, C., Zhang, J., Yang, J., & Liu, P.
- Affiliations
- First Affiliated Hospital of Xi'an Jiaotong University (CN)
- Roswell Park Comprehensive Cancer Center (US)
- Corresponding author
- Liu, Peijun
- ORCID
- Venue
- Scientific Reports
- Published
- 2017-02-07
- Volume
- 7
- Issue
- 1
- Pages
- 42125-42125
- ISSN
- 2045-2322 (ISSN-L)
- PMC
- PMC5294562
- OpenAlex
- W2586772947
- Cited by
- 61
- References
- 46
- Citations by year
- 2026: 3 · 2025: 6 · 2024: 5 · 2023: 8 · 2022: 5 · 2021: 7 · 2020: 14 · 2019: 7 · 2018: 6
- FWCI
- 3.94
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Scientific Reports (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (81502620, 81272342, 81502413)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Hippo pathway signaling and YAP/TAZ
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer-related molecular mechanisms research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Microtubule and mitosis dynamics
- Keywords
- DLG5, breast cancer, Hippo signaling pathway, YAP, epithelial-mesenchymal transition, epithelial polarity, Scribble, MST1, LATS1, TEAD transcription factors, cell proliferation, E-cadherin, N-cadherin, ZO-1
- MeSH terms
- Hippo Signaling Pathway, YAP-Signaling Proteins, TEA Domain Transcription Factors, Animals, Breast Neoplasms, DNA-Binding Proteins, Female, Humans, Membrane Proteins, Mice, Nude, Neoplasm Staging, Nuclear Proteins, Phosphoproteins, Proto-Oncogene Proteins, Transcription Factors, Transplantation, Heterologous, Signal Transduction, Antigens, CD, Cadherins, Gene Expression Regulation, Neoplastic, Cell Polarity, Hepatocyte Growth Factor, Protein Serine-Threonine Kinases, Tumor Suppressor Proteins, Cell Line, Tumor, Adaptor Proteins, Signal Transducing, Cell Proliferation, Epithelial-Mesenchymal Transition, MCF-7 Cells, Zonula Occludens-1 Protein, Carcinogenesis
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