Immune effector cells in the microenvironment tend to be depleted or remodeled, unable to perform normal functions, and even promote the malignant characterization of tumors, resulting in the formation of immunosuppressive microenvironments. The strategy of reversing immunosuppressive microenvironment has been widely used to enhance the tumor immunotherapy effect. Signal transducer and activator of transcription 3 (STAT3) was found to be a crucial regulator of immunosuppressive microenvironment formation and activation as well as a factor, stimulating tumor cell proliferation, survival, invasiveness and metastasis. Therefore, regulating the immune microenvironment by targeting the STAT3 oncogenic pathway might be a new cancer therapy strategy. This review discusses the pleiotropic effects of STAT3 on immune cell populations that are critical for tumorigenesis, and introduces the novel strategies targeting STAT3 oncogenic pathway for cancer immunotherapy. Lastly, we summarize the conventional drugs used in new STAT3-targeting anti-tumor applications.

Objective. To perform gene set enrichment analysis (GSEA) and analysis of immune cell infiltration on non-small-cell lung cancer (NSCLC) expression profiling microarray data based on bioinformatics, construct TICS scoring model to distinguish prognosis time, screen key genes and cancer-related pathways for NSCLC treatment, explore differential genes in NSCLC patients, predict potential therapeutic targets for NSCLC, and provide new directions for the treatment of NSCLC. Methods. Transcriptome data of 81 NSCLC patients and the GEO database were used to download matching clinical data (access number: GSE120622). Form the expression of non-small cell lung cancer (NSCLC). TICS values were calculated and grouped according to TICS values, and we used mRNA expression profile data to perform GSEA in non-small-cell lung cancer patients. Biological process (GO) analysis and DAVID and KOBAS were used to undertake pathway enrichment (KEGG) analysis of differential genes. Use protein interaction (PPI) to analyze the database STRING, and construct a PPI network model of target interaction. Results. We obtained 6 significantly related immune cells including activated B cells through the above analysis (Figure 1(b), $p<0.001$ ). Based on the TICS values of significantly correlated immune cells, 41 high-risk and 40 low-risk samples were obtained. TICS values and immune score values were subjected to Pearson correlation coefficient calculation, and TICS and IMS values were found to be significantly correlated (Cor = 0.7952). Based on non-small-cell lung cancer mRNA expression profile data, a substantial change in mRNA was found between both the high TICS group as well as the low TICS group (FDR 0.01, FC > 2). The researchers discovered 730 mRNAs that were considerably upregulated in the high TICS group and 121 mRNAs that were considerably downregulated in the low TICS group. High confidence edges (combined score >0.7) were selected using STRING data; then, 191 mRNAs were matched to the reciprocal edges; finally, an undirected network including 164 points and 777 edges was constructed. Important members of cellular chemokine-mediated signaling pathways, such as CCL19, affect patient survival time. Conclusion. (1) The longevity of patients with non-small-cell lung cancer was substantially connected with the presence of immature B cells, activated B cells, MDSC, effector memory CD4 T cells, eosinophils, and regulatory T cells. (2) Immune-related genes such as CX3CR1, CXCR4, CXCR5, and CCR7, which are associated with the survival of NSCLC, affect the prognosis of NSCLC patients by regulating the immune process.

Among all malignant tumors in the whole universe, the incidence and mortality of lung cancer disease rank first. Especially in the past few years, the occurrence of lung cancer in the urban population has continued to increase, which seriously threatens the lives and health of people. Among the many treatments for lung cancer, chemotherapy is the best one, but traditional chemotherapy has low specificity and drug resistance. To address the above issue, this study reviews the five biological pathways that common terpenoid compounds in medicinal plants interfere with the occurrence and development of lung cancer: cell proliferation, cell apoptosis, cell autophagy, cell invasion, metastasis, and immune mechanism regulation. In addition, the mechanism of the terpenoid natural traditional Chinese medicine monomer compound combined with Western medicine in the multipathway antilung cancer is summarized.

Colorectal cancer is a common clinical malignant tumor of the digestive tract, and intestinal flora has played an important role in the development of colorectal cancer. Bifidobacteria, as one of the main dominant florae in intestinal tract, can inhibit the occurrence and development of colorectal cancer through various mechanisms. Recent studies have shown that traditional Chinese medicine can regulate the abundance of bifidobacteria in intestinal tract and exhibit anti-tumor effects on colorectal cancer. Detailed investigations have revealed that the mechanisms of bifidobacteria in the treatment of colorectal cancer involve three aspects: the production of short-chain fatty acids, the regulation of the body's immunity, and the regulation of cell apoptosis and differentiation. In this review, we provide an updated summary of recent advances in our understanding of the mechanisms by which traditional Chinese medicine regulate intestinal flora to inhibit colorectal cancer development and metastasis.