Intracellular Calcium Affects Colon Cancer Cell Motility

Intracellular Calcium Affects Colon Cancer Cell Motility

shutterstock_155178920A calcium supplement a day may not make metastatic colon cancer go away. In fact, as reported in a new article from Gachon University in the Republic of Korea, dietary calcium supplementation may play a role in enhancing colon cancer cell metastasis.

“These results suggest that careful consideration may be given in deciding dietary calcium supplementation to patients undergoing treatment for metastatic cancer,” noted lead authors Dr. Pasupathi Sundaramoorthy and Dr. Jae Jun Sim. They, along with collaborators from different departments within the university conducted a study that identified a connection between focal adhesion kinase (FAK), cancer cell motility and calcium. Although all studies were conducted in vitro with human colon cancer cells, the results may have implications in humans with colon cancer.

To begin the study “Modulation of Intracellular Calcium Levels by Calcium Lactate Affects Colon Cancer Cell Motility through Calcium-Dependent Calpain,” which was published in PLoS One, the research team treated cells with calcium bound lactate (CaLa) and watched intracellular calcium levels. Calcium levels increased, as did cleavage of FAK, suggesting a role for downstreatm CaLa signaling in regulating cell adhesion and metastasis. An additional experiment showed the link was cleavage of FAK by caplain, a calcium-dependent protease.

The cleavage state of FAK is important because it determines whether or not FAK can enter the nucleus and affect gene transcription. According to the article, “cleaved FAK translocates into the nucleus,” promoting cancer cell survival by suppressing the tumor suppressor p53. Normally, p53 inhibits cell survival in damaged cells, which is an important preventative measure against tumor development.

Yet the effects of calcium on colon cancer cells do not end with FAK. The scientists also determined that CaLa enabled greater cell mobility. By treating cells with TAE226, a FAK inhibitor, the researchers were able to prevent CaLa-dependent cell migration.

Developing a FAK inhibitor such as TAE226 may be a better means of treating colon cancer than limiting dietary calcium intake. Calcium is an ion vital for normal cell functions and maintains the integrity of the skeleton. Without calcium, blood would not clot after receiving an incision in the skin.

However, just as with many other nutrients, too much calcium may have potential health risks. “Therefore, our results suggest that motility effects on colon cancer may be related to the use of calcium dietary supplementation,” stated the authors.

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