Dr Marina Kriajevska

Room 317
3rd Floor, Robert Kilpatrick Clinical Sciences Building
Leicester Royal Infirmary
PO BOX 65
Leicester LE2 7LX

Tel: +44 (0)116 229 7312 
Fax: +44 (0)116 252 3223
Email: mk108@le.ac.uk

Personal details

• MSc Biochemistry (Moscow State University, Russia)
• PhD Biochemistry (Institute of General Genetics, Moscow, Russia)

Publications

You can view my publications on PubMed.

Research

Metastatic dissemination is the main cause of mortality in cancer patients. Highly motile and invasive cells appear at different stages of tumour evolution, disseminate from the primary site and give rise to the secondary tumours. These motile tumour-initiating cells have properties of stem cells and are generated by abnormal activation of embryonic genetic programs termed Epithelial-Mesenchymal Transitions (EMT).

When EMT programs are activated in primary carcinomas, the affected cells lose their epithelial polarity, acquire a motile mesenchymal phenotype and escape from the original tumour. Several proteins belonging to ZEB, SNAIL or TWIST transcription factors families have been characterised as master regulators of EMT (EMT-TFs). EMTs are reversible, and modulations in the expression and the activity of EMT-TFs result in flexible changes in tumour cell phenotype.

My research is focused on tumour cell plasticity and, in particular, on how EMT affects cytoskeletal remodelling, cell morphology and motility. I use cancer xenograft models in Zebrafish for studying cell migration and invasion (collaboration with Dr Jonathan McDearmid, Leicester) (Fig.1). 

Gross alterations in gene expression patterns are molecular basis of EMT; and proteins of the S100 family are important EMT markers. I continue my research on the effect of S100 proteins on myosin dynamics and their implication in the development of EMT programs (Fig.2).

In collaboration with Dr Eugene Tulchinsky, I initiated a new project investigating the role of the receptor tyrosine kinase AXL in bladder cancer. AXL is activated in in vitro EMT models and overexpressed in EMT/stem-like subtypes of some cancers including transitional cell carcinoma of the bladder. Downregulation of AXL in bladder cancer cells significantly decreases cell invasion highlighting AXL as a potential therapeutic target molecule in bladder cancer (Fig.3).

Supervision

• Yiyang Sun, funded by MRC, September 2004 – September 2007
• Andrew Irvine, funded by BBSRC, December 2008 – December 2011
• Qais Al Ismaeel, funded by the Government of Iraq, October 2013 – October 2016
• Ban Alwash, funded by the Government of Iraq, January 2014 – January 2017
• Hanaa Al-Mahmoodi, funded by the Government of Iraq, April 2014 – April 2017
• Zamzam Almutairi, funded by the Government of Kuwait, March 2015 – March 2018

Academic Profile

•  Active member of the Biochemical Society and British Society for Cell Biology
• Member of the Editorial board member of Recent Patents on Anti-Cancer Drug Targets (IF: 3.5) & Scientific Reports (NPG, IF: 5.597)