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CDK1 is a normal protein that drives cells through the replication cycle, while MHC class 1 molecules are also normal molecules that present a small amount of protein on the cell surface for immune system examination. Recently, a study published in the international journal Cancer Research, scientists from the University of Colorado Cancer Center found that a group of cancer cells labeled with MHC class 1 molecule and high levels of CDK1 are extremely unusual. In fact, high levels of MHC class 1 molecule and CDK1 are usually the keys to certain diseases, such as melanoma, pancreatic cancer and colon cancer, and these cells may be the cancer stem cells that scientists have sought for a long time, once the cancer patient's treatment is finished, these cells become resistant to chemotherapy and re-sown the seeds of the cancer.
In the last post, we have introduced some of the research achievements in the RNA molecular biology research, here are another achievements that are related to RNA molecular research as well:
The Lasker Award, which is regarded as the ‘Wind Vane’ of the Nobel Prize. Professor Joan Argetsinger Steitz from Yale University won the 2018 Lasker Award for his 40 years of leadership in the field of bio-medicine, especially in the field of RNA biology. In this post, we will summarize the recent achievements in the field of RNA molecular biology research.
Life comes from a single cell (that is oosphere[oosperm]) that repeatedly divides to produce two cells, then four cells, then eight cells, up to about 26 billion cells that make up the newborn. A major challenge in developmental biology is to track how and when these 26 billion cells are produced from a fertilized egg. Until now, there are only snapshots for this developmental process being captured and analyzed in this field.
Tumor-microenvironment interactions play an important role in tumor progression, metastasis, and therapeutic resistance, and there is increasing evidence that tumor cell-derived exosomes can systematically regulate or reprogram tumor microenvironments through transferring molecules such as microRNAs, mRNAs, and proteins. PD-L1 is a classical immunological surface protein that inhibits the anti-tumor function of T cells by binding to receptor programmed cell death-1 (PD-1) and effectively protects tumors from immune surveillance. Exosomes are reported to contain certain types of proteins, including membrane proteins that promote cancer metastasis, such as EGFR and MET. As a membrane-bound protein, whether PD-L1 is present in cancer-derived exosomes, or playing a role in tumor progression remains unknown.
PD-L1 is a classical immunological surface protein that inhibits the anti-tumor function of T cells by binding to receptor programmed cell death-1 (PD-1) and effectively protects tumors from immune surveillance. For estimating the role of exo-PD-L1 in the tumor microenvironment and tumor progression in vivo, researchers measured tumor growth in 4T1-PD-L1 KO cells co-injected with EX-PD-L1 Flag, EX-PD-L1 KO or PBS. Consistent with previous reports, PD-L1 deficiency in 4T1-PD-L1 KO cells resulted in significant tumor regression, however, EX-PD-L1 Flag, but not EX-PD-L1 KO, significantly restored tumor growth in 4T1-PD-L1 KO cells. Then they exposed 4T1-PD-L1 KO cells to increasing amounts of EX-PD-L1 Flag, and the results showed that EX-PD-L1 Flag promoted tumor growth in a dose-dependent manner.
For a very long time, it has been thought that the neurodegenerative disorder of Alzheimer's disease is caused by β-amyloid plaques, which is called Amyloid Precursor Protein (APP), breaking down into fragments and accumulates in the brain to form misfolded, toxic polymers that impede neural communication. In the presence of Alzheimer's disease, β-amyloid plaques will lead to neuronal death directly, or destroy the nutritional supply of brain cells through the action of tau protein phosphorylation (tau protein bending to form neurofibrillary tangles), eventually killing them. However, a new study recently published in Stem Cell Reports by the University of Queensland, Australia suggested that we may need to rethink the biological mechanisms that lead to cognitive decline in Alzheimer's disease.
Recently, researchers at Northwestern University Medical School successfully prevented the growth of glioblastoma which was an invasive form of brain cancer by inhibiting an enzyme called CDK5. The related study has been published in the Journal of Cell Reports.
Recently, researchers from the Hollings Cancer Center at the University of Southern Carolina Medical School (MUSC) discovered that tumor cells use unfolded protein response (UPR) to change the biological clock, which further leads to tumor growth as a key part of the biological clock precisely inhibits the tumor growth process. Related study results being published in the Nature Cell Biology.
While mentioning about Shape-shifter, you may regard it as science fiction stuff, however, they really exist in our DNA. In a new study, researchers describe how two commonly mismatched bases in human DNA - guanine (G) and thymine (T) - can change shape, and thus creating an inconspicuous crosspiece on the DNA ladder, which allows them to survive by evading the body's natural defense against genetic mutations. Related research results were published online in the journal of Nature.
