Deregulation of Scribble Promotes Mammary Tumorigenesis and Reveals a Role for Cell Polarity in Carcinoma
Open accessAbstract
Loss of cell polarity proteins such as Scribble induces neoplasia in Drosophila by promoting uncontrolled proliferation. In mammals, the role that polarity proteins play during tumorigenesis is not well understood. Here, we demonstrate that depletion of Scribble in mammary epithelia disrupts cell polarity, blocks three-dimensional morphogenesis, inhibits apoptosis, and induces dysplasia in vivo that progress to tumors after long latency. Loss of Scribble cooperates with oncogenes such as c-myc to transform epithelial cells and induce tumors in vivo by blocking activation of an apoptosis pathway. Like depletion, mislocalization of Scribble from cell-cell junction was sufficient to promote cell transformation. Interestingly, spontaneous mammary tumors in mice and humans possess both downregulated and mislocalized Scribble. Thus, we demonstrate that scribble inhibits breast cancer formation and that deregulation of polarity pathways promotes dysplastic and neoplastic growth in mammals by disrupting morphogenesis and inhibiting cell death.
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Mutating Pro305 in the LRR to Leu (Scrib/P305L) abolishes membrane localization.
“Mutating Pro305 in the LRR12 to Leu (Scrib/P305L) abolishes membrane localization47,56,66,67.”
From Membrane recruitment of the polarity protein Scribble by the cell adhesion receptor TMIGD1 (2023) · cites this paper as [56]
The Results section reports that changing Scribble Pro305 to Leu (P305L) moved the protein from cell-cell junctions to the cytoplasm in mammary epithelial cells, supporting the localization claim. It identifies the LRR domain but does not specify that Pro305 lies in LRR12, as the citing sentence states. (LLM, conf=0.85)
Experimental — accuracy not yet measuredEctopic expression of Scrib/P305L in cell lines suppresses c-myc-induced apoptosis.
“Importantly, ectopic expression of Scrib/P305L in cell lines disrupts cell polarity, suppresses c-myc-induced apoptosis, enhances Akt signaling, and fails to suppress Ras-MAPK-induced EMT18,47,56,68.”
From Membrane recruitment of the polarity protein Scribble by the cell adhesion receptor TMIGD1 (2023) · cites this paper as [56]
The phenotype of ΔD1-TMIGD1-expressing cells strongly resembles the phenotype observed after depletion of Scrib in mammary gland-derived acinar epithelial cells and in lung organotypic cultures.
“a phenotype which strongly resembles the phenotype observed after depletion of Scrib in mammary gland-derived acinar epithelial cells56 and in lung organotypic cultures57.”
From Membrane recruitment of the polarity protein Scribble by the cell adhesion receptor TMIGD1 (2023) · cites this paper as [56]
Ectopic expression of Scrib/P305L in cell lines disrupts cell polarity.
“Importantly, ectopic expression of Scrib/P305L in cell lines disrupts cell polarity, suppresses c-myc-induced apoptosis, enhances Akt signaling, and fails to suppress Ras-MAPK-induced EMT18,47,56,68.”
From Membrane recruitment of the polarity protein Scribble by the cell adhesion receptor TMIGD1 (2023) · cites this paper as [56]
Ectopic expression of Scrib/P305L in cell lines enhances Akt signaling.
“Importantly, ectopic expression of Scrib/P305L in cell lines disrupts cell polarity, suppresses c-myc-induced apoptosis, enhances Akt signaling, and fails to suppress Ras-MAPK-induced EMT18,47,56,68.”
From Membrane recruitment of the polarity protein Scribble by the cell adhesion receptor TMIGD1 (2023) · cites this paper as [56]
The Results section on Scribble mislocalization reports that P305L-expressing cells lose polarity and resist Myc-induced apoptosis, but it does not report enhanced Akt signaling. Searches for Akt, P305L Akt phosphorylation, and Akt activation found no passage linking the mutant to Akt signaling in our copy. (LLM, conf=0.72)
Experimental — accuracy not yet measured
Ectopic expression of Scrib/P305L in cell lines fails to suppress Ras-MAPK-induced EMT.
“Importantly, ectopic expression of Scrib/P305L in cell lines disrupts cell polarity, suppresses c-myc-induced apoptosis, enhances Akt signaling, and fails to suppress Ras-MAPK-induced EMT18,47,56,68.”
From Membrane recruitment of the polarity protein Scribble by the cell adhesion receptor TMIGD1 (2023) · cites this paper as [56]
The Results section on Scribble mislocalization (page not provided) describes P305L-expressing mammary cells and shows that the mutant inhibits Myc-induced apoptosis. Searches for Ras-MAPK-induced EMT and epithelial–mesenchymal transition found no passage testing whether P305L suppresses that outcome. (LLM, conf=0.75)
Experimental — accuracy not yet measuredLoss of SCRIB expression functions as a tumor suppressor in Drosophila and mammals.
“Loss of SCRIB that results in uncontrolled proliferation and tissue growth identifying it as tumor suppressor (1).”
From Mislocalization of the Cell Polarity Protein Scribble Promotes Mammary Tumorigenesis and Is Associated with Basal Breast Cancer (2014) · cites this paper as [2]
In several human cancers-breast, prostate, and colon-hSCRIB protein is mislocalized away from cell-cell junctions.
“hSCRIB protein is mislocalized from cell-cell junctions in multiple human cancers, including breast, prostate and colon (2, 3).”
From Mislocalization of the Cell Polarity Protein Scribble Promotes Mammary Tumorigenesis and Is Associated with Basal Breast Cancer (2014) · cites this paper as [2]
In 3D MCF-10A cultures, wild-type hSCRIB overexpression did not affect morphogenesis, but hSCRIBP305L expression led to defective morphogenesis.
“overexpression of wild-type hSCRIB in MCF-10A mammary epithelial cells grown in 3D had no impact on morphogenesis, whereas expression of hSCRIBP305L displayed defective morphogenesis (2).”
From Mislocalization of the Cell Polarity Protein Scribble Promotes Mammary Tumorigenesis and Is Associated with Basal Breast Cancer (2014) · cites this paper as [2]
Loss or downregulation of SCRIB acts as a tumor suppressor by inhibiting cell death or inducing proliferation.
“Others and we have previously reported that downregulation (or loss) of SCRIB expression functions as a tumor suppressor by inhibiting cell death or inducing proliferation (2, 3).”
From Mislocalization of the Cell Polarity Protein Scribble Promotes Mammary Tumorigenesis and Is Associated with Basal Breast Cancer (2014) · cites this paper as [2]
hSCRIBP305L expression cooperates with Myc in transforming mammary epithelial cells.
“We have previously shown that expression of hSCRIBP305L cooperates with Myc during transformation of mammary epithelial cells (2).”
From Mislocalization of the Cell Polarity Protein Scribble Promotes Mammary Tumorigenesis and Is Associated with Basal Breast Cancer (2014) · cites this paper as [2]
c-myc induces both proliferation and apoptosis in mammary epithelial cells; the apoptosis function requires Scribble in complex with β-PIX and GIT1 to activate the Rac-JNK-JUN pathway.
“The expression of c-myc induces both proliferation and apoptosis in mammary epithelial cells, the latter function requiring Scribble, in complex with β-PIX and GIT1, to activate the Rac–JNK–JUN pathway.”
From Scribble: A master scaffold in polarity, adhesion, synaptogenesis, and proliferation (2019) · cites this paper as Zhan et al., 2008
Knockdown or mislocalization of Scribble was sufficient to override the proapoptotic signals from c-myc activation.
“Knockdown or mislocalization of Scribble was sufficient to override the proapoptotic signals from c-myc activation (Zhan et al., 2008).”
From Scribble: A master scaffold in polarity, adhesion, synaptogenesis, and proliferation (2019) · cites this paper as Zhan et al., 2008
In a transgenic transplantation mouse model for mammary carcinoma, loss of Scribble in conjunction with oncogenic activation of c-myc significantly enhances the size of tumors compared with activating c-myc alone.
“In a transgenic transplantation mouse model for mammary carcinoma, loss of Scribble in conjunction with oncogenic activation of c-myc significantly enhances the size of tumors compared with activating c-myc alone.”
From Scribble: A master scaffold in polarity, adhesion, synaptogenesis, and proliferation (2019) · cites this paper as Zhan et al., 2008
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- Authors
- Zhan, L., Rosenberg, A., Bergami, K. C., Yu, M., Xuan, Z., Jaffe, A. B., Allred, C., & Muthuswamy, S. K.
- Affiliations
- Cold Spring Harbor Laboratory (US)
- Memorial Sloan Kettering Cancer Center (US)
- Washington University in St. Louis (US)
- Corresponding author
- Muthuswamy, Senthil K.
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2008-11
- Volume
- 135
- Issue
- 5
- Pages
- 865-878
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC3015046
- OpenAlex
- W2086609648
- Cited by
- 436
- References
- 67
- Citations by year
- 2026: 10 · 2025: 9 · 2024: 11 · 2023: 29 · 2022: 14 · 2021: 14 · 2020: 14 · 2019: 19 · 2018: 22 · 2017: 25 · 2016: 29 · 2015: 25 · 2014: 26 · 2013: 31 · 2012: 43
- FWCI
- 16.64
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 1755 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Cold Spring Harbor Laboratory Institutional Repository (Cold Spring Harbor Laboratory) (acceptedVersion)
- Funders
- National Cancer Institute (CA105388, U01CA105388, CA098830, R56CA098830, R01CA098830)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Hippo pathway signaling and YAP/TAZ
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular Mechanics and Interactions
- Keywords
- Scribble, cell polarity, mammary carcinogenesis, breast cancer, apoptosis, c-Myc, cell transformation, dysplasia, cell-cell junction, protein mislocalization, tumor suppressor
- MeSH terms
- Animals, Breast Neoplasms, Epithelial Cells, Humans, Mammary Glands, Animal, Membrane Proteins, Down-Regulation, Mammary Neoplasms, Animal, Proto-Oncogene Proteins c-myc, Cell Polarity, Apoptosis, Tumor Suppressor Proteins, Cell Line, Tumor, Intracellular Signaling Peptides and Proteins, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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