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BACKGROUND: Gastric cancer (GC) ranks as the fifth most prevalent malignancy worldwide. Conventional treatments, including radiotherapy and chemotherapy, often induce severe side effects and significant adverse reactions, and they may also result in drug resistance. Consequently, there is a critical need for the development of new therapeutic agents. Traditional Chinese Medicine (TCM) and natural products are being extensively researched due to their low toxicity, multi-targeted approaches, and diverse pathways. Scholars are increasingly focusing on identifying active anticancer components within TCM. PURPOSE: This review aims to summarise research conducted over the past 14 years on the treatment of GC using TCM. The focus is on therapeutic targets, mechanisms, and efficacy of Chinese medicine and natural products, including monomer compounds, extracts or analogues, and active ingredients. METHODS: Relevant articles on TCM and GC were retrieved from PubMed using appropriate keywords. The collected articles were screened and classified according to the types of TCM, with an emphasis on the molecular mechanisms underlying the treatment of GC. RESULTS: The research on TCM indicates that TCM and natural products can effectively inhibit the metastasis, proliferation, and invasion of tumour cells. They can also induce apoptosis, autophagy and improve the chemosensitivity of drug-resistant cells. Additionally, injections derived from Chinese herbal medicine, when used as an adjunct to conventional chemotherapy, can significantly improve the prognosis of GC patients by reducing chemotherapy toxicity. CONCLUSION: This review summarises the progress of TCM treatment of GC over the past 14 years, and discusses its therapeutic application of GC, which proves that TCM is a promising treatment strategy for GC in the future.
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Background: Currently, there is few literature comprehensively analyzing landscape of cuproptosis-related genes (CRGs) in liver hepatocellular carcinoma (LIHC) with multiple omics approaches. Aims: Using comprehensive analysis, we aim to find out how CRGs works on LIHC. Method: With data from The Cancer Genome Atlas (TCGA) database, we constructed a prognostic prediction model for CGRs using LASSO regression analysis and performed immune infiltration analysis using the same dataset. To validate findings, we utilized RNA expression data from the International Cancer Genome Consortium (ICGC). Furthermore, we analyzed the enrichment and features of CRGs in epithelial cells using single-cell RNA sequencing (scRNA-seq) data. To validate the reliability of findings, we performed several experiments including RT-PCR, cloning formation assay, scratch assay, and Transwell assay. Result: We have constructed a high-precision risk scoring model composed of CRGs for predicting prognosis in TCGA-LIHC. Reliability of the risk prognosis model was confirmed through Kaplan-Meier curve analysis, time-dependent ROC analysis, and multivariate regression analysis. Furthermore, we found knocking down PDSS1 increased sensitivity of LIHC cells to copper ions, and both proliferation and migration abilities were significantly reduced. Finally, we comprehensively characterized the features of CRGs in LIHC through scRNA-seq. Conclusion: In this study, we introduce PDSS1 as a novel CRG in HCC. Utilizing scRNA-seq, we provide a comprehensive landscape of cuproptosis across various cell subtypes within the HCC tumor microenvironment. Furthermore, we detailed the characteristics of high PDSS1-expressing tumor cells, including their distinctive transcription factors, metabolic profiles, and interactions with different subtypes within the tumor microenvironment. This work not only elucidated the role of PDSS1 in HCC but also enhanced our understanding of cuproptosis dynamics during tumor progression.
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Radioiodine-refractory differentiated thyroid cancer (RAIR-DTC) is difficult to treat with radioactive iodine because of the absence of the sodium iodide transporter in the basement membrane of thyroid follicular cells for iodine uptake. This is usually due to the mutation or rearrangement of genes and the aberrant activation of signal pathways, which result in abnormal expression of thyroid-specific genes, leading to resistance of differentiated thyroid cancer cells to radioiodine therapy. Therefore, inhibiting the proliferation and growth of RAIR-DTC with multikinase inhibitors and other drugs or restoring its differentiation and then carrying out radioiodine therapy have become the first-line treatment strategies and main research directions. The drugs that regulate these kinases or signaling pathways have been studied in clinical and preclinical settings. In this review, we summarized the major gene mutations, gene rearrangements and abnormal activation of signaling pathways that led to radioiodine resistance of RAIR-DTC, as well as the medicine that have been tested in clinical and preclinical trials.