EMMPRIN在肺癌介导的抑制成骨分化过程中的作用及机制研究.docx

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Abstract
Cancer-induced bone disease (CIBD) is a common complication that occurs in advanced stages of lung cancer. EMMPRIN, a glycoprotein expressed on the cell surface of cancer cells, has been shown to play an important role in the progression of CIBD. In this paper, we review the current understanding of the role of EMMPRIN in inhibiting osteogenic differentiation processes and the mechanisms by which it exerts its effects. A comprehensive understanding of this process could provide novel therapeutic targets for the prevention and treatment of CIBD in lung cancer patients.
Introduction
CIBD is a common complication that occurs in late-stage lung cancer patients, and it is characterized by osteolytic lesions leading to bone pain, pathological fracture, and hypercalcemia (1). The mechanisms underlying CIBD involve the interaction between cancer cells and bone cells, and recent studies have shown that EMMPRIN plays an important role in this process.
EMMPRIN, also known as CD147, is a cell surface glycoprotein that is expressed on the surface of many cancer cells, including lung cancer. It is involved in a wide range of cellular processes, including cell adhesion, migration, invasion, and angiogenesis (2). In addition, EMMPRIN has been shown to be involved in the regulation of bone metabolism, and its expression has been found to be upregulated in osteoclasts, osteoblasts, and mesenchymal stem cells (3).
EMMPRIN and Inhibition of Osteogenic Differentiation Processes
Recent studies have shown that EMMPRIN plays a key role in inhibiting osteogenic differentiation processes in bone cells (4, 5). This process involves the interaction between EMMPRIN and various signaling pathways involved in osteoblast differentiation, such as the Wnt/β-catenin pathway.
The Wnt/β-catenin pathway is essential for the differentiation, proliferation, and function of osteoblasts, which are responsible for bone formation (6). Wnt signaling activates β-catenin, which then translocates into the nucleus and binds to target gene promoters, such as Runx2, to promote osteoblast differentiation (7). EMMPRIN has been shown to inhibit the Wnt/β-catenin pathway in osteoblasts, thus inhibiting their differentiation.
Moreover, EMMPRIN has also been shown to induce the expression of osteoclast differentiation factors, which promote the differentiation of osteoclasts, leading to bone resorption (8). In addition, EMMPRIN can directly activate osteoclasts, leading to the production of cytokines that promote osteoclast differentiation (9).
Mechanisms of EMMPRIN-induced inhibition of osteogenic differentiation
There are several potential mechanisms by which EMMPRIN inhibits osteogenic differentiation. First, EMMPRIN has been shown to affect the expression and activation of various signaling pathways involved in osteoblast differentiation, such as the Wnt/β-catenin pathway, the BMP pathway, and the Hedgehog pathway (10, 11). By inhibiting these pathways, EMMPRIN can suppress osteoblast differentiation.
Second, EMMPRIN has been shown to directly interact with extracellular matrix molecules, such as integrins, leading to the activation of intracellular signaling pathways that negatively regulate osteoblast differentiation (12).
Third, EMMPRIN has been shown to activate the NF-κB signaling pathway, which is involved in inflammation and osteoclast differentiation (13). The activation of this pathway can promote osteoclast differentiation and bone resorption.
Therapeutic Strategies Targeting EMMPRIN
Given the important role of EMMPRIN in the inhibition of osteogenic differentiation processes, it is a potential target for therapeutic intervention in CIBD. There are several strategies that can be used to inhibit the activity of EMMPRIN, including the use of monoclonal antibodies and small molecule inhibitors (14).
Monoclonal antibodies targeting EMMPRIN have been shown to be effective in reducing tumor growth and metastasis in preclinical studies (15). In addition, small molecule inhibitors targeting EMMPRIN have also been developed, and some have shown promising results in preclinical studies (16).
Conclusion
In conclusion, EMMPRIN plays an important role in inhibiting osteogenic differentiation processes in bone cells, leading to the development of CIBD in lung cancer patients. A comprehensive understanding of the mechanisms underlying EMMPRIN-induced inhibition of osteogenic differentiation processes could provide novel therapeutic targets for the prevention and treatment of CIBD in lung cancer patients.