The mechanism of macrophage promoting the development of polymorphic glioblastoma is revealed.

On July 19th, the international academic journal Molecular Cell published the latest research results of the Yang Yanwei Research Group at the Institute of Biochemistry and Cell Biology of the Chinese Academy of Sciences: Macrophage-associated PGK1 phosphorylation promotes saerobic glycolyis and tumorigenesis.
the study revealed that tumor-related macrophages regulate the glytic solution of tumor cells by regulating the phosphorylation of PGK1 in tumor cells, thus promoting the development of polymorphic glioblastoma.
tumor microenvironment is a complex environment on which tumor cells depend, and is composed of many different extracellular matrix and matrix cells.
tumor-related macrophages (Tumor-associated macrophages, TAMs) are the macrophages immersed in tumor tissue and are the largest number of immune cells in the tumor microenvironment.
studies have shown that tumor-related macrophages can promote tumor cell growth and metastasis in a variety of ways, but it is not clear whether they can regulate tumor cell metabolism.
the latest research from Yang's group, TAMs secrete lemetry 6 (interleukin 6, IL6) on glioma cells, promoting the protein kinasse 1 (3-phosphoinosiste-dependent protein) in glioma cells, PGK1 243th bit sines (T243).
the affinity of PGK1 and substrates after
PGK1 T243 phosphorylation, which promotes the activity of pgK1 glycoenzyme, and promotes the aerobic sugar enzyme, cell proliferation and tumor growth of glioma cells.
can inhibit the aerobic sugar enzyme, cell proliferation, and tumor growth of TAMs-promoted glioma cells by using IL6 neutralizing antibodies, inhibiting PDPK1 activity in tumor cells or PGK1 T243 phosphorylation.
by immunizing samples of glioma patients, the researchers found that PGK1 T243 phosphorylation was closely related to The expression of PDPK1 activity, TAMs immersion, and IL6;
the work for the first time revealed a new mechanism by which macrophages in the microenvironment can promote tumor growth by regulating tumor cell metabolism, a new model of protein translation modification to the catalytic direction regulation of metabolic enzymes was established, and PGK1 T243 phosphorylation was suggested to act as a biomarker indicating the progoma prognosis, and new strategies were provided for the treatment of glioma, namely, the inhibition of the phosphadization of PGK1 to cut off the connection between TAMs and tumor cells. Li Guohui, a researcher at the Dalian Institute of Chemical Physics of the Chinese Academy of Sciences,
, co-author of the paper.
Yang Weiwei, Ph.D. student Zhang Yaxuan, Professor Yu Guanzhen and Dr. Chu Huixuan of Dalian Chemical Institute are the co-first authors of the paper.
the research work was funded by the National Natural Science Foundation of China, the Strategic Priority Research Project of the Chinese Academy of Sciences and the Youth Thousand Stakes Program.
the research data collection is supported by the Molecular Platform and Animal Platform of the Public Technical Service Center for Biochemistry and Cell.
macrophages regulate the direction of PGK1 catalysis by secreting IL6 to induce PDPK1-mediated PGK1 phosphorylation in tumor cells, thus enhancing the glysaclysis of tumor cells and ultimately promoting the malignant progression of tumors.
.