Professor Sima Lev: Epithelial–Mesenchymal Transition: EMT
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This document discusses the role of the protein Nir2 in epithelial-to-mesenchymal transition (EMT) and cancer metastasis. It finds that Nir2 expression modulates cell morphology and positively regulates EMT, migration, and invasion. Knocking down Nir2 in a breast cancer cell line results in fewer metastatic nodules in a mouse model. The document also examines the expression of Nir2 in human breast tumors and discusses its role in affecting cancer metastasis.
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Professor Sima Lev: Epithelial–Mesenchymal Transition: EMT
- 1. Loss of Apico-Basal Polarity Gain of Mesenchymal Proteins Vimentin Fibronectin N-cadherin a-SMA b-Catenin E-cadherin Cytokeratin ZO-1 Lamin-1 a/g-catenin
- 2. MDA-MB-231/EGF MDA-MB-231/10% FBS Nir2 regulates cell migration & invasion
- 3. Nir2 expression modulates cell morphology
- 4. Nir2 positively regulates EMT
- 6. MDA-MB-231 (tail vain injection) Control Nir2 KD Nir2 KDControl Numberofnodules Nir2 affects cancer Metastasis
- 7. Expression of Nir2 in breast tumors Keinan. et al, J. Cell Science 2014 n=286 Expression of VAPB in breast tumors Rao. et al, PlosOne 2012
- 8. Breast, Melanoma, Colon Breast Cancer PITPNC1 promotes metastasis of multiple cancer types Proposed Model
- 9. The StAR-related lipid transfer proteins F. Alpy & C. Tomasetto JCS, 118, 2791, 2005 Cholesterol Cholesterol PC Cholesterol/25Hc PC/PE Ceramide STARD3-silencing results in cell growth arrest and apoptosis in HER2-positive cell lines. How STARD3 contributes to the phenotype of HER2 cancers is still unclear. LE Cholesterol transport LE-to-ER STARD3 modifies the distribution and morphology of LE LE-ER MCSs reducing the maturation of LE and fusion to lysosome Inhibition of RTKs degradation (HER2)
- 10. SUMMARY LTPs transfer lipids according to the lipid composition of their target membrane Mechanistic Insight underlying lipid transfer by LTPs LTPs coordinate the level of different lipid species at specific membrane domains Cytokinesis, cell growth, migration, EMT Physiological roles Neurodegeneration, cancer & metastasis Pathological implications Regulation? Post translation modifications? Interacting proteins? Targeting?
Editor's Notes
- EMT a crucial developmental process implicated in organ development, tissue repair, and organ fibrosis, plays a major role in cancer progression, invasion and metastasis EMT is defined by the loss of epithelial characteristics and the acquisition of a motile, invasive and migratory mesenchymal phenotype This conversion is accompanied by loss of cell-cell adhesion and cell polarity, decrease in the expression of epithelial markers such as E-cadherin, increase in the expression of mesenchymal markers such as vimentin, fibronectin, N-cadherin, alpha-smooth muscle actin (α-SMA), as well as increase in the activity of matrix metalloproteinases
- STARD3 was isolated in the early 1990s in a study aimed at finding new genes implicated in breast cancer. The function of the STARD3 gene, referred to at that time as Metastatic Lymph Node clone number 64 (MLN64), remained a mystery until the discovery of the steroidogenic acute regulatory protein (StAR/STARD1). STARD3 gene lied next to the oncogene HER2/ERBB2 on chromosome 17q11-12. STARD3 was indeed co-amplified and co-expressed with HER2 in about 25 % of breast cancers. A second insight into STARD3’s function came from the identification of its subcellular localization at the membrane of late endosomes [12 ] and from its bi-functional protein structure