Dr Elena Rainero
School of Biosciences
Lecturer
+44 114 222 3696
Full contact details
School of Biosciences
B2-04, Florey Building
Firth Court
Western Bank
ºù«Ӱҵ
S10 2TN
- Profile
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- 2016–present: Lecturer, ºù«Ӱҵ (UK)
- 2015–2016: Research Fellow, ºù«Ӱҵ (UK)
- 2009–2015: Post-doctoral researcher, the Beatson Institute for Cancer Research, Glasgow (UK)
- Qualifications
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- 2010: PhD in Human Biotechnology, University of Piemonte Orientale, Novara (Italy)
- 2006: Master Degree in Medical and Pharmaceutical Biotechnology, 110/110 cum laude, University of Piemonte Orientale, Novara (Italy)
- 2004: Bachelor Degree in Biotechnology, 110/110 cum laude, University of Piemonte Orientale, Novara (Italy)
- Research interests
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My group is interested in understanding the role of extracellular matrix internalisation in invasive cell migration and cell growth.
The extracellular matrix (ECM) is a complex network of secreted proteins that, beyond providing physical support to organs and tissues, regulates many cell functions, including proliferation, polarity, migration and oncogenic transformation.
Our aims are to understand the basic molecular events regulating ECM endocytosis, as well as how ECM uptake impinges on invasive cell migration and proliferation in complex 3D environments.
Extracellular matrix internalisation in breast cancer
The extracellular matrix (ECM) is a complex network of secreted proteins which not only provides tissue support, but is also involved in the control of several cell functions, including migration and oncogenic transformation.
The tumour microenvironment has a pivotal role in modulating cancer initiation, progression and metastasis, while cancer cells in turn modify the composition and properties of the ECM, demonstrating a bi-directional interaction between tumour and stroma.
Our research addresses cell-ECM interaction from a novel and exciting angle, investigating how the internalisation of ECM components control breast cancer cell invasion.
Using a combination of different approaches, we aim at characterising the molecular mechanisms controlling ECM internalisation and how this process impinges on cancer cell growth and invasion.
The role of the extracellular matrix in supporting breast cancer cell metabolism
Altered cellular metabolism is one of the hallmarks of cancer. Due to tumour growth rate and limited blood supply, the tumour microenvironment is often hypoxic and deprived of nutrients (including glucose and amino acids).
Cancer cells have been shown to use extracellular protein to support nutrient signalling and cell growth; however, the contribution of a complex 3D extracellular matrix (ECM) and its endocytosis to cancer cell growth and metabolism is very unclear.
Our lab is characterising the contribution of the extracellular matrix in fuelling breast cancer cell growth in 3D environments.
Our preliminary data indicate that the presence of a collagen I, matrigel or laminin/entactin matrix is sufficient to rescue breast cancer cell growth in nutrient deprived conditions, in a way that requires ECM endocytosis.
Interestingly, the ECM promotes cell growth/survival in the absence of amino acids or glucose, but not in serum, suggesting that the lack of specific nutrients can be compensated, at least in part, by the ECM.
Furthermore, the ECM promotes cell proliferation under glutamine and amino acid starvation, but not serum or glucose. Taken together, these data suggest that the ECM can sustain cell growth/survival through different mechanisms depending on the specific starvation conditions.
We hypothesise that, under nutrient-deprived conditions, breast cancer cells use ECM internalisation and breakdown to support their proliferation/survival.
To investigate this, we are assessing the contribution of complex 3D matrices and ECM receptors to cancer cell growth and elucidating whether ECM trafficking is driven by nutrient starvation.
We will define how ECM internalisation impinges on cell metabolism and nutrient signalling and whether ECM-dependent
growth is promoted during carcinoma progression.
- Publications
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Show: Featured publications All publications
Featured publications
Journal articles
- . PLOS Biology, 22(1).
- . Frontiers in Oncology, 10.
- . International Journal of Experimental Pathology.
- . Nature Communications, 8.
- . Biochemical Society Transactions, 44(5), 1347-1354.
- . Cell Reports, 10(3), 398-413.
- . Developmental Cell, 23(3), 560-572.
- . The Journal of Cell Biology, 196(2), 277-295.
- . PLOS Biology, 22(12), e3002930-e3002930.
All publications
Journal articles
- . Cancer Research, 84(10), 1543-1545.
- . Current Opinion in Cell Biology, 88, 102359-102359.
- . PLOS Biology, 22(1).
- . Diseases & Research, 4(1), 40-52.
- . Cancers, 14(6).
- . Frontiers in Oncology, 10.
- . Essays In Biochemistry.
- . International Journal of Experimental Pathology.
- . Nature Communications, 8.
- . Nature Communications, 8.
- . Biochemical Society Transactions, 44(5), 1347-1354.
- . Nature Cell Biology, 17(11), 1373-1375.
- . Cell Reports, 10(3), 398-413.
- . Journal of Cell Science, 127(18), 3893-3901.
- . BioEssays, 35(6), 523-532.
- . Cancer Research, 72(22), 5801-5811.
- . Developmental Cell, 23(3), 560-572.
- . The Journal of Cell Biology, 196(2), 277-295.
- . Cellular Signalling, 23(12), 1988-1996.
- . The Journal of Immunology, 187(11), 5941-5951.
- . Science Signaling, 4(171), pe24-pe24.
- . European Journal of Cancer Supplements, 8(5), 190-191.
- . Proceedings of the National Academy of Sciences, 107(9), 4182-4187.
- HGF induces cell migration, ruffling and Rac activation through a novel signalling pathway coupling diacylglycerol kinase alpha to PKCz/i and RhoGDI. FEBS JOURNAL, 276, 250-250.
- . Oncogene, 27(7), 942-956.
- DIACYLGLYCEROL KINASE ALPHA IS REQUIRED FOR PROLIFERATION AND INVASION INDUCED BY GROWTH FACTORS AND CHEMOKINES. ANTICANCER RESEARCH, 28(5C), 3302-3303.
- . Molecular Biology of the Cell, 18(12), 4859-4871.
- . PLOS Biology, 22(12), e3002930-e3002930.
- . PLoS ONE, 9(6).
- .
Chapters
Conference proceedings papers
- Unravelling extracellular matrix endocytosis in breast cancer. INTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY, Vol. 101(3-4) (pp A4-A4)
- . Cancer Research, Vol. 77(4 Supplement), 6 December 2016 - 10 December 2016.
- CLIC3 controls delivery of late endosomal MT1-MMP to the ventral plasma membrane and dictates invasion and metastasis in estrogen receptor-negative breast cancer. EUROPEAN JOURNAL OF CANCER, Vol. 50 (pp S112-S112)
- Diacilglycerol kinase alpha regulates central lumen formation through Annexin2 and Cdc42. FEBS JOURNAL, Vol. 278 (pp 141-141)
- Diacylglycerol kinase alpha regulates SDF1 alpha-induced cell invasion by regulating atypical PKC and matrix metallo proteinases 9. FEBS JOURNAL, Vol. 277 (pp 124-124)
- Diacylglycerol Kinase alpha mediates HGF-induced Rac activation and membrane ruffling by regulating atypical PKC and RhoGDI. FEBS JOURNAL, Vol. 277 (pp 124-124)
Preprints
- Research group
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We advertise PhD opportunities (Funded or Self-Funded) on FindAPhD.com
- Teaching activities
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Undergraduate:
- BMS243 module co-ordinator
- BMS243/247 Stem cells, aging and cancer
- BMS379 Cancer Biology
- Level 3 Practical and Dissertation Modules