ArticleCancer cell international2016
Suppression of Spry4 enhances cancer stem cell properties of human MDA-MB-231 breast carcinoma cells.
Article in Cancer cell international, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 24 citations in OpenAlex.
- Mdm2 requires Sprouty4 to regulate focal adhesion formation and metastasis independent of p53.Nature communications · 2024Article
- Role of SPRY4 in health and disease.Frontiers in oncology · 2024Review
- Sprouty4 is epigenetically upregulated in human colorectal cancer.Epigenetics · 2023Article
- SPRY4 inhibits and sensitizes the primary KIT mutants in gastrointestinal stromal tumors (GISTs) to imatinib.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2023Article
- Sprouty 4 expression in human oral squamous cell carcinogenesis.Journal of dental sciences · 2023Article
- The risk model construction of the genes regulated by H3K36me3 and H3K79me2 in breast cancer.Biophysics reports · 2023Article
- The prognostic significance of human ovarian aging-related signature in breast cancer after surgery: A multicohort study.Frontiers in immunology · 2023Article
- The dynamic broad epigenetic (H3K4me3, H3K27ac) domain as a mark of essential genes.Clinical epigenetics · 2021Review
- Article
- Sprouty4 negatively regulates ERK/MAPK signaling and the transition from in situ to invasive breast ductal carcinoma.PloS one · 2021Article
- Article
- Commonly integrated epigenetic modifications of differentially expressed genes lead to adaptive resistance in cancer.Epigenomics · 2019Article
- Oncogenic microRNA-411 promotes lung carcinogenesis by directly targeting suppressor genes SPRY4 and TXNIP.Oncogene · 2019Article
- MicroRNA‑181 serves an oncogenic role in breast cancer via the inhibition of SPRY4.Molecular medicine reports · 2018Article
- Knockdown of SPRY4 and SPRY4-IT1 inhibits cell growth and phosphorylation of Akt in human testicular germ cell tumours.Scientific reports · 2018Article
- Ganoderma lucidum polysaccharide inhibits prostate cancer cell migration via the protein arginine methyltransferase 6 signaling pathway.Molecular medicine reports · 2018Article
- ITIH5 mediates epigenetic reprogramming of breast cancer cells.Molecular cancer · 2017Article
- Erratum to: Suppression of Spry4 enhances cancer stem cell properties of human MDA-MB-231 breast carcinoma cells.Cancer cell international · 2017Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundCancer stem cells contribute to tumor initiation, heterogeneity, and recurrence, and are critical targets in cancer therapy. Sprouty4 (Spry4) is a potent inhibitor of signal transduction pathways elicited by receptor tyrosine kinases, and has roles in regulating cell proliferation, migration and differentiation. Spry4 has been implicated as a tumor suppressor and in modulating embryonic stem cells.
objectivesThe purpose of this research was to test the novel idea that Spry4 regulates cancer stem cell properties in breast cancer.
methodsLoss-of function of Spry4 in human MDA-MB-231 cell was used to test our hypothesis. Spry4 knockdown or control cell lines were generated using lentiviral delivery of human Spry4 or non-targeting control shRNAs, and then selected with 2 μg/ml puromycin. Cell growth and migratory abilities were determined using growth curve and cell cycle flow cytometry analyses and scratch assays, respectively. Xenograft tumor model was used to determine the tumorigenic activity and metastasis in vivo. Cancer stem cell related markers were evaluated using immunoblotting assays and fluorescence-activated cell sorting. Cancer stem cell phenotype was evaluated using in vitro mammosphere formation and drug sensitivity tests, and in vivo limiting dilution tumor formation assay.
resultsTwo out of three tested human Spry4 shRNAs significantly suppressed the expression of endogenous Spry4 in MDA-MB-231 cells. Suppressing Spry4 expression increased MDA-MB-231 cell proliferation and migration. Suppressing Spry4 increased β3-integrin expression, and CD133(+)CD44(+) subpopulation. Suppressing Spry4 increased mammosphere formation, while decreasing the sensitivity of MDA-MB-231 cells to Paclitaxel treatment. Finally, suppressing Spry4 increased the potency of MDA-MB-231 cell tumor initiation, a feature attributed to cancer stem cells.
conclusionsOur findings provide novel evidence that endogenous Spry4 may have tumor suppressive activity in breast cancer by suppressing cancer stem cell properties in addition to negative effects on tumor cell proliferation and migration.
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