In the 20th century, scientists began learn more about the cellular and molecular mechanisms that drive the progression of cancer. With the continuous progress of biomedical research, the function of cells can be directionally changed, thus providing innovative methods for scientific research and medical disease detection and research, and developing new methods for the treatment of critically ill patients. Cancer is characterized by the loss of critical cellular function caused by specific genetic mutations. Cancer may occur in any organ of the body and may form a solid tumor or a tumor that affects blood cells. Malignant tumors and tumors are also often used to describe cancer. In 1970, scientists discovered the first identified viral oncogene of SRC. The protein encoded by SRC is tyrosine protein kinase. in many animal species and humans, SRC mutation is associated with the malignant development of colon, liver, lung, breast and pancreatic cancer. Not only that, there are many cancer-related proteins and their receptor proteins in life, and then follow us to learn about several typical cancer-related receptor proteins.
Summary of tumor Necrosis Factor TNF Family and its receptor basis.
Figure 1. TNF Superfamily Receptions
Tumor necrosis factor (TNF)
Tumor necrosis factor (TNF) is a cytokine found in the serum that kills cancer cells in mice. The tumor necrosis factor superfamily has been found to include 19 ligands and 29 different receptors. Members of the tumor necrosis factor TNF superfamily specifically recognize 29 receptors to form a ligand-receptor interaction system. Tumor necrosis factor TNF superfamily has many important physiological and pathological functions. TNF causes tumor cell necrosis and apoptosis. TNF plays a key role in various immune and inflammatory processes, including cell activation, survival, proliferation, necrosis and apoptosis. TNFR is mainly a transmembrane protein and participates in some physiological processes, such as host defense, inflammation, apoptosis, autoimmunity, immunity, ectoderm and nervous system development and organogenesis. TNFR plays an important role in immune response, for example, FASLAPO2L/TRAIL induces apoptosis through p53 independent mechanism. The members of tumor necrosis factor TNF superfamily are related to tumorigenesis, tumor development, invasion and metastasis. The role of TNF superfamily in immune, cardiovascular, neurological, pulmonary and metabolic diseases is becoming more and more obvious, and it is the main goal of drug development.
Toll-like Receptors and Tumor Immunology
Figure 2. Toll-like Receptors
Toll-like receptors are mammalian homologues of Drosophila Toll protein and are recognized as the most important pattern recognition receptors in innate immunity. During pathogen infection, Toll-like receptors recognize pathogens by binding to pathogen-related molecular pattern (PAMPs). Activated Toll-like receptors activate downstream cascade signals, promote the secretion of cytokines and chemical factors, and finally activate innate and adaptive immune responses to eliminate pathogens. Toll-like receptors are the first barrier of innate immunity, and they also play an important role in immune surveillance and regulation in the occurrence and development of tumors. Different Toll-like receptor signals in tumor cells show completely different activity of immunosuppression or tumor immune escape. Some Toll-like receptors are beneficial to tumor development, and these Toll-like receptor signals induce pro-inflammatory responses. It should be able to promote the formation of tumor microenvironment, and then promote the formation of tumor. But some Toll-like receptor signals can kill tumor cells by indirectly activating the tolerant host immune system.
Under the influence of external environment, cells often have gene mutations, and the process of malignant transformation of mutated cells is monitored by the immune system. Toll-like receptors, as the first barrier of the innate immune system, monitor and identify specific ligands from different sources and regulate the immune response. The growth of malignant transformed cells in the body can provide danger signals recognized by the immune system, including malignant transformed cell-related endogenous substances and tumor antigens. These danger signals can be specifically recognized by Toll-like receptors and activate antigen-presenting cells to promote tumor-associated antigens. The differentiation and maturation of heterosexual T cells activate the tumor immune response of the immune system. On the contrary, if the Toll-like receptor is inactivated or absent, the immune system will lose its response to the tumor and enter the tumor immune tolerance state. In the process of tumorigenesis, some endogenous ligands are released, and through the binding of Toll-like receptors to cause chronic inflammatory response, recruit inflammatory cells, including neutrophils, DC cells, NK cells and tumor-related macrophages, to induce the immune response to tumor.
Figure 3. TLR1,TLR2,TLR4,TLR5 and TLR6 are both receptors on the cell surface, TLR3, TLR7, TLR 8 and TLR9 are located in the connotation body, and TLR11 only exists in mice.
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HER-2 / Neu
HER-2 / neu (erbB-2) is a gene that encodes human epidermal growth factor receptor type 2. There are moderate amounts of this receptor on some normal cells. The combination of this gene with growth factors under appropriate conditions can stimulate cell division. In human breast cancer cases, up to 30% of cases have amplification of the HER-2 / neu gene. Increasing the number of HER-2 / neu gene copies can lead to higher expression of HER-2 protein on the cell surface, resulting in faster cell proliferation. It is currently believed that gene amplification will affect the ability of tumors to grow and spread, as well as tumor response to treatment. Overexpression of this gene can make tumors more aggressive, but it can also make tumors more sensitive to some chemotherapy drugs.
A recent study involved 140 patients with primary breast tumors using a combination of two chemotherapeutic drugs at different concentrations. The results show that cells with stronger HER-2 / neu expression are more susceptible to chemotherapeutic drugs than cells with weaker expression, and tumor growth is more inhibited. HER-2 / neu expansion seems to make tumor cells sensitive to chemotherapeutic drugs, rather than making them resistant. Chemotherapy drugs attack cells that are replicating genes, and HER-2 / neu amplification leads to faster replication. Therefore, it can be concluded that tumor cells that overexpress HER2 will be more effectively killed because of the faster cell division.
Epidermal growth factor receptor (EGFR) is a transmembrane protein. It has a portion outside the cell, then crosses the surface of the cell, and stretches out to the cytoplasm. It functions as a cellular antenna. When a specific protein binds to EGFR, two epidermal growth factor receptor proteins stick to each other. In many cancers, the EGFR gene is mutated or overactive. These cancers include breast cancer, lung cancer, esophageal cancer, and head and neck cancer. 16 In cancer cells and other cells present in tumors, excessive activity of EGFR can lead to blood vessel growth, excessive cell division, enhanced cell survival and cell movement, leading to the spread of cancer.