UC Berkeley study finds new insight into cancer cell multiplication

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Campus molecular and cell biology researchers found that melanoma cells become immortal via a two-step process, as revealed in their research paper published Thursday.

The Hockemeyer and Tijan-Darzacq Labs conducted the research in collaboration with researchers at UC San Francisco. Their research sheds more light on the early stages of cancer development, according to Dirk Hockemeyer, a campus assistant professor of cell and developmental biology.

According to David McSwiggen, a campus doctoral student in molecular and cell biology and a paper collaborator, the human body has safeguards in place to keep cells from growing out of control, limiting these cells in their ability to multiply.

A hallmark of cancer cells is a mutation that was believed to give cells an unlimited ability to multiply through cell division, according to Franziska Lorbeer, one of the main authors of the study. This study, however, found that the mutation is actually only the first step in cancer cell immortalization.

According to Lorbeer and Kunitoshi Chiba, the second main author of the paper, because the mutation that leads to telomerase activation is found in a variety of cancers, these findings could be used to better understand other cancers, such as glioblastoma.

“This study addresses the very early steps of tumorigenesis that are not well understood,” Chiba and Lorbeer said in an email. “It is intriguing to speculate how that could affect tumor formation.”

McSwiggen said in an email that the group sought to determine the impact of this mutation by measuring telomeres in various cancer cells. Telomeres, a key part of the study, are parts of DNA that shorten every time cells divide, according to McSwiggen.

“The length of a cell’s telomeres can then be thought of as a molecular counter that says how many (times) a cell can divide before its telomeres become too short, and it enters a crisis and dies,” McSwiggen said in an email. “Cancers often avoid this crisis by reactivating telomerase — an enzyme that extends telomeres.”

The group specifically examined the lengths of telomeres of benign tumor cells and cancerous tumor cells, according to McSwiggen. Hockemeyer added that after comparing their lengths, the group concluded that the immortalization of cancer cells is not solely caused by the the initial enzyme mutation.

While the group looked only at melanoma cells, Hockemeyer said he strongly believes that the findings in this study can be generalized to other types of cancers. Hockemeyer added that the group does not yet know what the second step is, only that the initial mutation is not enough and that the new findings warrant more study of tumor biology.

“It means that we have to better understand the early biology of cancer development,” Hockemeyer said.

Michael Lee is the lead research and ideas reporter. Contact him at [email protected] and follow him on Twitter at @_HyunkyuL.