new progress!The Liangguang team of Hangzhou Medical College revealed the molecular mechanism of BORIS repair cell DNA damage

Recently, Zhang Yanmei, Professor Liang Guang of Hangzhou Medical College, published a research paper at the international TOP journal "Molecular Cancer" magazine (Zone 1 of the Chinese Academy of Sciences, IF = 41). in Cancer. The study revealed the molecular mechanism of the cancer protein BORIS generally expressed in tumor tissue to guide the abnormal DNA repair of cancer cells, and for the first time reported the BTAPEP-TAT of the BORIS function that targets the function of cancer protein. The first unit of the paper is Hangzhou Medical College. The first authors are Zhang Yanmei and Fang Mengdie of the Inspection Medical College (School of Biological Engineering), respectively, and the author of the joint communications are Zhang Yanmei and Liang Guang, respectively.

BORIS protein is expressed in almost all types of tumor tissues, but it is not expressed in the corresponding normal tissue. The existence of BORIS also leads to multi -medicinal resistance for lung cancer, colorectal cancer, brain cancer and other cancers. BORIS's lack or expression reduces the development of cancer cell proliferation and the occurrence of cancer, but the molecular mechanism is unknown. Due to the lack of inhibitors that targeted BORIS, the analysis of BORIS functions and its clinical application research have been obtained for a long time.

The study screened a polypeptide BTAPEP-TAT with a specific combination and inhibiting the BORIS function. BTAPEP-TAT combines BORIS's N-end amino acids to induce cancer cell apoptosis and DNA damage, and alleviate the development of non-small cell lung cancer. On this basis, the research team used BTAPEP-TAT to study the function of BORIS's damage to cancer cell DNA. The research team found that BORIS could promote the repair of single or double-chain DNA damage in cancer cells, while BTAPEP-TAT inhibits BORIS inhibitory and causes cancer cell DNA damage. Further studies have found that the nucleosogene basis modification in the BORIS protein 198-228AA response to DNA damage in the cancer cells, and BORIS's nucleosogenesis raised KU70 to participate in the damage to DNA in the cells. BORIS protein 198-228AA in the paradoxicization on glutamic acid in the section of glutamic acid is the key cause of repairing DNA damage in cancer cells. BTAPEP-TAT's inhibitory inhibitory modification of nucleosogene basis modification in the BORIS 198-228AA section is the main cause of killing cancer cells.

BORIS ribetose -based modification The mechanism diagram of the mechanism for promoting cancer cell DNA injury repair

The study first discovered the type and key amino acid position of the translated and key amino acid positioning of the Cancer cell DNA damage repair function on BORIS protein, and the mechanism of decrypting the cancer protein BORIS in the cancer cells; The inhibitory peptide provides a basis for clinical use of BORIS diagnosis of cancer, and also provides pre -body drugs and evaluation methods for targeting BORIS cancer therapy.

(Source: Hangzhou Medical College Scientific Research Office)

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