Tracking Biointerfacial Cellular/Molecular Cues for Cancerous Progression of Stem Cells
Stacey Mont
Major: Molecular Biology
Mentor: Dr. Kiminobu Sugaya, Molecular Science Center
Stacey Mont was born in Tampa, Fl. Her research interests include cancer stem cell biology. In addition to research through the McNair program, she has done summer research through Rutgers University's Research in Science and Engineering Program (RISE) and the IGERT Summer Undergraduate Research Frontiers (ISURF) program. She is interested in molecular biology and cancer cell biology graduate programs.
The following abstract is from research conducted at Rutgers, The State University of New Jersey (New Brunswick Campus), and at UMDNJ-Robert Wood Johnson Medical School, as part of the Research in Science and Engineering (RISE) summer program, as well as the NSF-IGERT Summer Undergraduate Research Frontiers (ISURF) program. It was conducted in conjunction with Er Liu, under the guidance of Dr. Prabhas V. Moghe (Biomedical Engineering Department) and Dr. Hak-Joon Sung (The New Jersey Center for Biomaterials), with support from the UCF McNair Scholars Program, FASEB MARC Program, Merck Research Labs, Celgene Corp, and Johnson & Johnson.
As early as the late 1960s, scientists have hypothesized that the origin of cancer and tumorgenesis may be due to a sub-population of adult stem cells. Adult stem cells do not divide as rapidly as cancer cells and thus are not affected by chemotherapy targeted to rapidly proliferating cells. However, there remains a group of precursor cells within every population of adult stem cells. We hypothesize that such precursor cells may progressively convert into sarcoma lineage under certain molecular or biomaterials-related microenvironments. The hypothesis was tested by monitoring the progression into osteosarcoma of human Mesenchymal Stem Cells (hMSCs) and of their osteogenic precursors (OPs). The change in expression of specific protein markers and their morphological variance were examined in three distinct configurations of co-cultures designed to modulate the differentiating capacity of the hMSCs and OPs into osteosarcoma. The culturing techniques used were: Transwell systems (disall wing direct contact but enabling paracrine signaling), randomly co-cultured cells allowing direct cell-to-cell contact using hMSCs or OPs with SAOS-2 cells, and conditioning by culturing hMSCs and OPs with conditional SAOS-2 media. Preliminary results indicate that Topoisomerase II appears to be a selective marker for osteosarcoma progression. Also a morphological affect was observed in hMSCs/OPs when co-cultured with SAOS-2 cells. Future studies will focus on determining if hMSCs/OPs express more Topoisomerase II in the co-culture system as well as quantifying morphometric descriptors of cytoskeletal organization. The results from the current research program may yield a greater understanding of how osteosarcoma develops and occurs, which in turn may help guide more molecularly targeted cancer therapies.