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Tumor Suppressors

Tumor Suppressors Background


The occurrence of cancer is caused by many factors. The development of normal cells to cancer cells is a multi-process. Proto-oncogenes acquire new characteristics due to mutations, such as excessive activity, which will promote the further development of cancer. The most common cancers involve the inactivation of specific tumor suppressor genes and the activation of certain proto-oncogenes. In contrast to the protein encoded by the proto-oncogene, the product of the tumor suppressor gene is another gene that exists in cells under normal conditions and can inhibit cell growth. If it loses its function, it may promote tumor transformation of cells. These cancer-promoting genes are called oncogenes. Their negatively regulated counterparts, genes that encode proteins that prevent cancer, are called tumor suppressors. Once these tumor suppressors are lost due to mutations, overphosphorylation, or promoter methylation, cancers grow uncontrollably. Therefore, tumorigenesis may be the result of oncogene activation and inactivation of tumor suppressor genes. Currently, the two most famous tumor suppressor genes are the Rb gene and the p53 gene.

p53 bound to DNA p53 prevents cancer formation and acts as a guardian of the genome. Mutations in the p53 gene contribute to about half of the cases of human cancer. Figure 1. p53 bound to DNA p53 prevents cancer formation and acts as a guardian of the genome. Mutations in the p53 gene contribute to about half of the cases of human cancer.

Their products are nuclear proteins that control cell growth in the form of transcriptional regulators. Other tumor suppressor genes include neurofibromatosis-1 gene, colon adenoma polyp gene and colon cancer loss gene. We provide proteins encoded by a variety of tumor suppressor genes. The goal is to provide a variety of high-quality tumor suppressors to help researchers complete better research results.

DNA damage response signaling pathways target p53 and its key regulators Figure 2. DNA damage response signaling pathways target p53 and its key regulators (Meek DW, et al. 2009)

Tumor Suppressor Proteins

To date, more than 70 tumor suppressors of varying importance have been identified. Some are lost late in tumorigenesis and are considered "passenger mutations" that have little or no survival advantage over existing cancers. Other tumor suppressors are lost in the early stages of tumor neoplasia, and this loss is essential for the evolution from normal cells to cancer cells. These "driver gene mutations" occur in current tumor suppressor genes, each of which protects the integrity of the cellular processes that are essential for maintaining normal cells. These are the major tumor suppressors. Fully described examples of tumor suppressor proteins include p53 and retinoblastoma.

Scientific Research of Tumor Suppressor Proteins

The function of tumor suppressor proteins has been studied by many scientists, Studies have shown that tumor suppressor proteins play a key role in suppressing infections. The researchers found that when the functional tumor suppressor protein Arl11 gene was inserted into lung cancer cells, the cells died. Researchers have performed experiments in mouse and human cultured cells and found that Arl11 is essential for macrophages to be able to detect and destroy pathogens. When they encounter bacteria, they turn on Arl11 in macrophages. Silencing Arl11-expressing macrophages activates other immune cells. When macrophages are infected with Salmonella, those bacteria lacking Arl11 cannot stop the bacteria from multiplying. Arl11 appears to work by initiating a signal cascade called the ERK / MAP kinase pathway, which is known to regulate cell division and is therefore associated with cancer. People with von Hippel–Lindau (VHL) disease develop hemangiomas (hematoblastomas) of the brain and eyes, as well as tumors of the kidneys and adrenals. When the remaining copies of normal VHL genes are inactivated, tumors form. VHL mutations are also common in kidney cancer in the general population, but these mutations are acquired spontaneously. pVHL attaches chemical polyubiquitin to certain proteins in the cell. The marker is recognized by a cellular machine called the proteasome, which degrades proteins. The best understood pVHL target is the protein hypoxia-inducible factor, which controls genes turned on by hypoxia. In order for pVHL to target HIF for destruction, the presence of oxygen is required. In the absence of oxygen (or in tumor cells lacking normal pVHL), HIF accumulates and activates genes that promote survival in low oxygen environments. Some of these genes direct the synthesis of proteins that induce angiogenesis.

These studies show that tumor suppressor proteins have an indispensable role in the occurrence of cancer and the occurrence of biophysiology. Therefore, tumor suppressor proteins have also become an advantageous research tool for scientific researchers. Creative BioMart offers a variety of sources, grades and formulations of cancer suppressors for your research applications.


  1. Arya S B, Kumar G, Kaur H, et al. ARL11 regulates lipopolysaccharide-stimulated macrophage activation by promoting mitogen-activated protein kinase (MAPK) signaling. Journal of Biological Chemistry, 2018, 293(25): 9892-9909.
  2. Meek D W. Tumour suppression by p53: a role for the DNA damage response. Nature Reviews Cancer, 2009, 9(10): 714.


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