Metastasis, or the formation of secondary tumors, leads to majority of deaths related to cancer. The exact mechanism for how this works in cells that are far removed from a cancer’s primary tumor, remains an area of ongoing cancer research.
In a new study, researchers from University of Minnesota Twin Cities (UMTC) found an explanation for the century-old hypothesis for how cancer forms hybrids within the body, leading to metastasis.
They found a link between healthy-tumor hybrid cells and metastatic tumors for the first time, studying their distinct heterogeneous gene expression profiles found in human hybrid cells and how these hybrid cells form spontaneously
Researchers at UMTC cultured healthy cells & tumor cells, which spontaneously fused to form hybrids. Using the technique called RNA-seq, they then took a molecular snapshot of the gene expression of each fused hybrid cell. The resulting hybrids were found to express the genes of both the healthy cell and the tumor cell. It was found that this aids metastatic cells in surviving the primary tumor and potentially helping lay the groundwork for other tumor cells.
When hybrids are formed, cytoplasmic and nuclear material of two cells are forced to reorganize into one cell. Some of these cells can start proliferating and moving more actively than their parent cells. It was only in recent years the more advanced sequencing technology helped understand and tackle this challenge.
Cancer research community recognizes the fact that it is this cell heterogeneity that makes it hard to treat all tumors. It is not always possible to create different therapies to target different tumor cell types. If the factors that cause tumor heterogeneity are checked at the source, by limiting the hybrid formation – it will be a big development in cancer treatment.
Researchers hope their findings will lead to more research on how hybrids are formed, helping in drug development to inhibit hybrid formation, which might prevent metastatic spread of cancer.