Discovery of a new mechanism for cell division that can prevent cancer cell development and proliferation

Researchers in Korea have discovered a new cell division mechanism induced by beta-catenin, a protein in the human body. Through this, it is expected to contribute greatly to the development of anticancer drugs that induce cancer generation and suppression of cancer cell proliferation caused by abnormal cell division in the future.

The study, conducted by Dr. Lee Kyung-ho’s team at the Korea Biotechnology Research Center (Director Kim Jang-sung, hereinafter referred to as Life Research Institute), was supported by major projects of the Korea Biotechnology Institute, and creative fusion research projects promoted by the Ministry of Science and ICT and the Korea Research Foundation.

Cell division is known to be the cause of cancer due to the basic characteristics of living organism survival or abnormal proliferation of cells deviating from normal cell division. Cell division is a process in which one parent cell divides and multiplies into two or more daughter cells (cells divided into new cells), and is an essential process for the survival of cells, which are the basic constituent units of all living organisms.

Cell division can be divided into mitosis and meiosis, where one cell produces two daughter cells in one division for cell proliferation, and one cell produces four daughter cells in two divisions to make reproductive cells. Mitosis occurs sequentially in the process of fission and cytoplasmic division, and the cytoplasmic division of animal cells is divided into two daughter cells after the surface of the cell equatorial plate enters into small pieces (cytoplasmic indentation). As such, if cell division continues to proliferate abnormally quickly due to the basic characteristics of living organisms’ survival or certain factors, the mechanism of cell division becomes an important starting point in the development of anticancer drugs.

The research team found that beta-catenin protein, one of the main factors in wint signaling, is a key factor in regulating cytoplasmic division, the last process of cell division. To date, various factors and mechanisms for cell division have been reported, but much of the research on the process of dividing into two cells in cytoplasmic division has not been known. Through experiments, the research team found that serine No. 60, one of the amino acids that make up beta-catenine, induces cytoplasmic indentation when phosphorylated by a specific phosphorylase (Polo-like kinase 1, Plk1), regulating cytoplasmic division, the last process of cell division.

In addition, as a result of applying this mechanism to several cancer cells, the research team confirmed that the proliferation of cancer cells is significantly reduced when preventing the phosphorylation of beta-catenin No. 60 serin, and that beta-catenin is a decisive factor in cancer cell proliferation. This fact can be said to provide a mechanism that can control cell division through phosphorylation control of beta-catenin, and furthermore, can be an important target for the development of anticancer drugs that can suppress cancer development or cancer proliferation caused by cell division abnormality.

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Image: Phosphorylation of β-catenin Ser60 by Plk1 in cooperation with Ect2 induces RhoA activation and mediates the progression of furrow ingression and subsequent cytokinesis steps.

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