ArticleMolecular cancer research : MCR2014
The SmgGDS splice variant SmgGDS-558 is a key promoter of tumor growth and RhoA signaling in breast cancer.
Article in Molecular cancer research : MCR, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- A bioinformatic survey of RNA isoform diversity and expression across 9 GTEx tissues using long-read sequencing data.BMC genomics · 2025Article
- RHOA lactylation at oncogenic hotspots promotes oncogenic activity and protein stabilization.Molecular cancer · 2025Article
- The Many Roads from Alternative Splicing to Cancer: Molecular Mechanisms Involving Driver Genes.Cancers · 2024Review
- Structural and biophysical properties of farnesylated KRas interacting with the chaperone SmgGDS-558.Biophysical journal · 2022Article
- SmgGDS: An Emerging Master Regulator of Prenylation and Trafficking by Small GTPases in the Ras and Rho Families.Frontiers in molecular biosciences · 2021Review
- Splice switching an oncogenic ratio of SmgGDS isoforms as a strategy to diminish malignancy.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Structural Insights into the Regulation Mechanism of Small GTPases by GEFs.Molecules (Basel, Switzerland) · 2019Review
- GEF mechanism revealed by the structure of SmgGDS-558 and farnesylated RhoA complex and its implication for a chaperone mechanism.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- SmgGDS-607 Regulation of RhoA GTPase Prenylation Is Nucleotide-Dependent.Biochemistry · 2018Article
- Sema4C/PlexinB2 signaling controls breast cancer cell growth, hormonal dependence and tumorigenic potential.Cell death and differentiation · 2018Article
- Hypoxia leads to significant changes in alternative splicing and elevated expression of CLK splice factor kinases in PC3 prostate cancer cells.BMC cancer · 2018Article
- Article
- Structure-based analysis of the guanine nucleotide exchange factor SmgGDS reveals armadillo-repeat motifs and key regions for activity and GTPase binding.The Journal of biological chemistry · 2017Article
- Metazoan evolution of the armadillo repeat superfamily.Cellular and molecular life sciences : CMLS · 2017Article
- The Tumor-suppressive Small GTPase DiRas1 Binds the Noncanonical Guanine Nucleotide Exchange Factor SmgGDS and Antagonizes SmgGDS Interactions with Oncogenic Small GTPases.The Journal of biological chemistry · 2016Article
- Minireview: Mouse Models of Rho GTPase Function in Mammary Gland Development, Tumorigenesis, and Metastasis.Molecular endocrinology (Baltimore, Md.) · 2016Review
- The chaperone protein SmgGDS interacts with small GTPases entering the prenylation pathway by recognizing the last amino acid in the CAAX motif.The Journal of biological chemistry · 2014Article
- SmgGDS-558 regulates the cell cycle in pancreatic, non-small cell lung, and breast cancers.Cell cycle (Georgetown, Tex.) · 2014Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
unlabelledBreast cancer malignancy is promoted by the small GTPases RhoA and RhoC. SmgGDS is a guanine nucleotide exchange factor that activates RhoA and RhoC in vitro. We previously reported that two splice variants of SmgGDS, SmgGDS-607, and SmgGDS-558, have different characteristics in binding and transport of small GTPases. To define the role of SmgGDS in breast cancer, we tested the expression of SmgGDS in breast tumors, and the role of each splice variant in proliferation, tumor growth, Rho activation, and NF-κB transcriptional activity in breast cancer cells. We show upregulated SmgGDS protein expression in breast cancer samples compared with normal breast tissue. In addition, Kaplan-Meier survival curves indicated that patients with high SmgGDS expression in their tumors had worse clinical outcomes. Knockdown of SmgGDS-558, but not SmgGDS-607, in breast cancer cells decreased proliferation, in vivo tumor growth, and RhoA activity. Furthermore, we found that SmgGDS promoted a Rho-dependent activation of the transcription factor NF-κB, which provides a potential mechanism to define how SmgGDS-mediated activation of RhoA promotes breast cancer. This study demonstrates that elevated SmgGDS expression in breast tumors correlates with poor survival, and that SmgGDS-558 plays a functional role in breast cancer malignancy. Taken together, these findings define SmgGDS-558 as a unique promoter of RhoA and NF-κB activity and a novel therapeutic target in breast cancer. IMPLICATIONS: This study defines a new mechanism to regulate the activities of RhoA and NF-κB in breast cancer cells, and identifies SmgGDS-558 as a novel promoter of breast cancer malignancy.
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