Remove two proteins, or change the way DNA is repaired

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All organs in the human body are composed of cells, and orderly cell growth and differentiation can meet the needs of the body and maintain good health. However, if the cells continue to divide, an extra large number of cells can form tumors. Malignant cells invade and destroy adjacent tissues and organs. Also, cancer cells can penetrate the tumor and enter the blood or lymphatic system to form cancer metastases

According to statistics, the incidence rate of cancer patients in China is the highest in the world. About 4.57 million people are diagnosed with cancer every year, and about 3 million people die each year due to cancer. Almost 10,000 people die because of cancer every day. . Undoubtedly, cancer has become a major killer of life.

Repairing DNA damage is critical for keeping cells healthy and preventing cancer. Researchers at the University of Birmingham have discovered a new way for cancer cells to repair DNA damage, pointing to two previously unidentified proteins involved in DNA repair, SETD1A and BOD1L.

We know that many tumors are resistant to radiation and chemotherapy. Finding drugs that can sensitize tumors to treatment is a life-saver for cancer patients to achieve desired outcomes, and one way to sensitize tumors to treatment is to target cells that repair damaged DNA.

During DNA replication, the DNA double strands are unwound and replicated separately to produce new DNA double strands. During this process, the DNA replication complex is in an unstable state. These unstable structures, newly synthesized DNA strands, and replication forks are susceptible to degradation. SETD1A, on the other hand, stabilizes newly generated DNA by regulating histone methylation.

The study also identified another uncharacterized factor associated with newly replicated chromatin, BOD1L. Following replication stress, cells lacking BOD1L accumulate damaged genes that manifest as excessive chromosomal breaks. But BOD1L does not regulate spindle orientation, but rather has a protective effect.

The SETD1A and BOD1L proteins in the study modify other proteins called histones, and the modified proteins bind to DNA. Experiments have shown that removing these two proteins changes how DNA is repaired and makes cancer cells more sensitive to radiation therapy.

Overall, the new findings reveal novel responses of cancer cells to chemotherapy and radiation, which could lead to more targeted treatments for cancer patients in the future.