ArticleBMC cancer2019
Deletion of sorting nexin 27 suppresses proliferation in highly aggressive breast cancer MDA-MB-231 cells in vitro and in vivo.
Article in BMC cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 26 citations in OpenAlex.
- Targeting sorting nexin 3 to treat pulmonary fibrosis by dual modulating Wnt/β-catenin signaling.Cell death & disease · 2026Article
- SNX14 inhibits autophagy via the PI3K/AKT/mTOR signaling cascade in breast cancer cells.Journal of molecular histology · 2024Article
- Adaptations of membrane trafficking in cancer and tumorigenesis.Journal of cell science · 2024Review
- Review
- Inverse Impact of Cancer Drugs on Circular and Linear RNAs in Breast Cancer Cell Lines.Non-coding RNA · 2023Article
- Review
- HPV-18E6 Inhibits Interactions between TANC2 and SNX27 in a PBM-Dependent Manner and Promotes Increased Cell Proliferation.Journal of virology · 2022Article
- Sorting nexin 3 induces heart failure via promoting retromer-dependent nuclear trafficking of STAT3.Cell death and differentiation · 2021Article
- Toward Understanding the Molecular Role of SNX27/Retromer in Human Health and Disease.Frontiers in cell and developmental biology · 2021Review
- Sorting Nexin 27 as a potential target in G protein‑coupled receptor recycling for cancer therapy (Review).Oncology reports · 2020Review
- Interplay Between SNX27 and DAG Metabolism in the Control of Trafficking and Signaling at the IS.International journal of molecular sciences · 2020Review
- tRNA Queuosine Modification Enzyme Modulates the Growth and Microbiome Recruitment to Breast Tumors.Cancers · 2020Article
- SNX27-retromer assembly recycles MT1-MMP to invadopodia and promotes breast cancer metastasis.The Journal of cell biology · 2020Article
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundSorting Nexin 27 (SNX27) belongs to a family of sortin nexins and possesses a unique binding domain at the C-terminus which mediates protein-protein interaction in intracellular trafficking, membrane remodeling, organelle motility, and tight junctions. However, its role in cancer development, especially in vivo, remains largely unknown.
methodsWe have generated a stable SNX27 knockdown clone in a highly aggressive breast cancer cell line MDA-MB-231 using an inducible lentiviral shRNA system. Cell migration and proliferation of SNX27 knockdown (KD) cells were compared with wild-type (WT) cells by MTT and wound healing assay, respectively. The differences in colony formation between SNX27-KD and WT cells were detected by soft agar culture and matrigel 3D culture. Furthermore, tumor growth was examined in a xenograft nude mouse model using SNX27-KD and WT MDA-MB-231 cells. The critical EMT (epithelial-mesenchymal transition) regulators were examined in vitro and in vivo.
resultsThe wound healing assay showed that SNX27 knockdown significantly decreased cell motility and proliferation. Colony formation in soft agar showed that the SNX27 knockdown cells formed significantly fewer and smaller colonies than the parental MDA-MB-231 cells. Western blots and immunostaining showed that knockdown of SNX27 led to increased expression of E-cadherin and β-catenin proteins, which facilitate adhesion formation and reverse EMT. EMT is a cellular program that allows polarized, immotile epithelial cells to convert to motile mesenchymal cells, promoting carcinoma invasion. The expression levels of Vimentin, the transcription factor of EMT, and tight junction protein Claudin-5, were significantly diminished in the SNX27 knockdown cells. The expression of PCNA, the cell proliferation marker, was increased in SNX27-KD cells transfected with E-cadherin siRNA. In a xenograft nude mouse model, we found that knockdown of SNX27 significantly inhibited tumor growth. The tumors from mice with SNX27-KD cells showed less proliferation compared to tumors from mice injected with wildtype cells. The increase in E-cadherin and β-catenin and decrease in Vimentin and Claudin-5 were observed in tumors of mice injected with SNX27-KD cells.
conclusionsOur data have demonstrated that SNX27 plays a crucial role in tumor growth in vitro and in vivo.
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