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In China， malignant tumors have become the main cause of death. In the past half century， the incidence and mortality of malignant tumors have been on the rise， posing a threat to health of patients， and the burden of cancer has been increasing. At the moment， malignant tumors are mainly treated by surgery， radiotherapy， and cytotoxic drugs， which， however， have limitations and induce great adverse reactions. As biological technology and the research on tumor microenvironment， immunology， cell biology， and molecular biology advance， high-efficiency low-toxicity targeted therapy has attracted wide attention in the treatment of tumors. Epidermal growth factor receptor （EGFR） plays an important role in many cellular processes such as cell proliferation， survival， differentiation， migration， inflammation， and stromal homeostasis. EGFR promotes tumor growth， proliferation， and metastasis in a variety of ways. Chinese medicine has unique efficacy in the comprehensive treatment of malignant tumors. Through multiple components， multiple targets， and multiple pathways， it enhances the efficacy， reduces toxicity， prolongs life， and improves life quality in the treatment of tumors. Many Chinese medicines and their active components exert anti-tumor effect by inhibiting the EGFR signal transduction pathway. Through targeted inhibition of EGFR， Chinese medicine can promote the apoptosis and autophagy of tumor cells， suppress the proliferation and metastasis of tumor cells， and delay the progression of tumors. Thus， EGFR is a potential target for suppressing tumor. This paper summarizes the relationship between EGFR signal transduction pathway and tumor occurrence and development and analyzes the anti-tumor action mode and possible mechanisms of Chinese medicine and the active components by regulating EGFR signaling pathway， which is expected to provide a reference for clinical practice.
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Objective:To investigate the effects of myeloid differentiation protein-2 (MD-2) on paclitaxel resistance cells in triple negative breast cancer (TNBC) through EGFR signaling pathway.Methods:Immunohistochemical method was used to detect the expression of MD-2 in cancer tissue and adjacent tissue of TNBC patients, and the relationship between MD-2 expression and clinicopathological parameters of patients was analyzed. The TNBC paclitaxel-resistant cell line was constructed and MD-2 expression in cells was interfered. Cell invasion was detected by Transwell, and cell apoptosis was detected by flow cytometry. The signaling pathways regulated by MD-2 were screened by transcriptome sequencing and verified by Western blot.Results:The expression of MD-2 was significantly enhanced in cancer tissues relative to adjacent tissues. High expression of MD-2 was closely related to clinical stage, tumor size, tumor recurrence and metastasis ( χ2=4.50, P=0.032; χ2=2.55, P=0.011; χ2=4.40, P=0.036). In cell experiments, compared with normal breast cells, the expression of MD-2 in TNBC cell lines was significantly enhanced. Compared with sh-NC group (100±11.52) (6.81±0.57), knockdown of MD-2 could inhibit the invasion (61.44±6.78) ( t=4.99, P=0.008) but promote apoptosis (15.19±1.06) ( t=12.06, P<0.001) of paclitaxel resistant TNBC cells. Transcriptome sequencing and Western blot results showed that MD-2 mainly affects the biological behavior of TNBC cells by regulating the EGFR signaling pathway. Conclusions:MD-2 promoted TNBC cell invasion and paclitaxel resistance, which may be achieved by affecting the EGFR signaling pathway. MD-2 is expected to become an effective target in TNBC treatment.
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ADAMs is a family of transmembrane proteins with multi domains and multiple functions,which play important roles in many(patho-)physiological processes.They are upregulated in a variety of tumors and possess protein shedding and adhesive activities,which showed that they could be useful as tumor biomarkers and promising targets for designing new anti-tumor drugs.This review focuses on the roles ADAMs play in the process of tumor development and the potential application in cancer therapy.