Chinese and Western medicine have different understandings of the tumor microenvironment and different treatment methods.
The concept of the tumor microenvironment has been widely accepted. In the theory of Chinese and Western medicine, the concept of tumor microenvironment is similar, but there are still differences. Tumor treatment strategies for tumor microenvironment are receiving increasing attention.
Modern medical research on cancer shows that hepatocellular carcinoma (HCC) is related to tumor microenvironment. Studying the relationship between tumor microenvironment and HCC can be used as a new research direction to provide more strategies and ideas for the prevention and treatment of HCC. This article describes the characteristics of tumor microenvironment, cytokines, related signaling pathways, the occurrence and development of traditional Chinese medicine and HCC, and treatment-related knowledge.
Quercetin self-nanoemulsifying drug delivery system promotes apoptosis of SMMC-7721 cells in vitro.
Quercetin self-nanoemulsifying drug delivery system inhibits the expression of STAT3 and Survivin in SMMC-7721 cells.
This study describes the role of Quercetin in promoting apoptosis of SMMC-7721. Quercetin self-nanoemulsifying drug delivery system can also be used as a drug carrier, which providing ideas for precise treatment.
Objective: To study the mechanism of inhibition of SMMC-7721 liver cancer cells by quercetin self-nanoemulsifying drug delivery system (Q-SNEDDS) in vitro. Methods: The inhibitory effect of Q-SNEDDS on hepatoma cells was detected by MTT assay. The effect of Q-SNEDDS on apoptosis of hepatoma cells was detected by flow cytometry. The changes of Q-SNEDDS after hepatoma cells were observed by fluorescence microscopy. The effect of Q-SNEDDS on the expression of signal transduction and activator of transcription 3 (STAT3) and anti-apoptotic factor (survivin) protein in hepatoma cells was examined by Immunohistochemistry. Results: Q-SNEDDS significantly inhibited the proliferation of hepatoma cells in a concentration-dependent manner. After 24 h of Q-SNEDDS treatment, the total apoptosis rate was 25.8%; STAT3 and survivin protein expression was down-regulated in the Q-SNEDDS group. Conclusion: Q-SNEDDS may play a role in inducing apoptosis by inhibiting the expression of STAT3 and survivin proteins.
Network pharmacology is a new science and is becoming a new way for TCM study.
Network pharmacology combines with TCM is a new medical research model.
The network pharmacology approach is capable of describing complex interactions among biological system, drugs, and diseases, such as cancer from a network perspective. It helps us to understand how herbal medicine works on people with cancer and how a new indication of a given herbal formula can be predicted.
Traditional Chinese Medicine (TCM) emphasizes integrity and systematicity. Chinese Herbal Medicine (CHM) is characterized by multi-component, multi-target, multi-channel complex action. Cancer belongs to polygenic disease, and it is characteristic of complex traits of the disease which is determined by multiple genes. Network pharmacology integrates disease network, drug network, and biological system network, analyzes the interaction among diseases, drugs and specific nodes in the network, and studies the pathogenesis of cancer, the action mechanism of drugs and compatibility principle of prescription. In the field of cancer, by applying concepts and methods of network pharmacology, we are expected to find new type drugs-“biological networks regulatory drug”. It is helpful for individualized treatment, improved prognosis, and therapeutic effect.
Highlights: In this paper, various factors related to Hashimoto’s thyroiditis and thyroid cancer, especially papillary thyroid cancer, morbidity and lymph node metastasis, are reviewed concerning recent literature.
Editor’s Summary: In recent decades, it is very high for the incidence of HT and the thyroid cancer rate. This article is more likely that autoimmune thyroid inflammation such as HT is carcinogenic, and thyroid dysfunction related to HT may also promote tumor growth induced by stimulating TSH receptor.
Abstract: In recent years, the incidence of Hashimoto’s thyroiditis and thyroid cancer has shown a rapid growth trend. These two diseases have severely affected the public health. Many epidemiological studies have shown that thyroid cancer is often associated with Hashimoto’s thyroiditis. Hashimoto’s thyroiditis may promote the occurrence of thyroid cancer, as well as affecting the progression of the tumor, lymph node metastasis, and even the prognosis of patients. In this paper, the relationship between Hashimoto’s thyroiditis and thyroid cancer and the pathogenesis of thyroid cancer are reviewed regarding molecular mechanism, clinical pathology, and serology.
The proceeding of cancer development seems to be driven by the complex interaction among cells, stroma and adjacent tissue. Here we advocate a new conception, cancer field, to describe the development of cancer, a complex adaptive system. Cancer field may be divided into center of tumor, periphery of tumor and adjacent tissue. The balance of inhibitors and inducers, including the interaction among cancer cells, niche and adjacent tissue, governs the switch of development of cancer field, which mimic embryonic development, a dynamic process of self-organization. The radial component of intra-tumor heterogeneity raises the field change effects in cancer field. Research strategy may be changed from single cancer cell to cancer field, from malignant transform to cancer development biology. Highlights：The proceeding of cancer development seems to be driven by the complex interaction among cells, stroma and adjacent tissue. Here we advocate a new conception, cancer field, to describe the development of cancer, a complex adaptive system. Editor’s Summary：The radial component of intra-tumor heterogeneity raises the field change effects in cancer field. Research strategy may be changed from single cancer cell to cancer field, from malignant transform to cancer development biology.
Copyright © TMR Publishing Group.
E-mail: TMRCancer@tmrjournals.com | https://www.tmrjournals.com/cancer