Objective Marvelous advancements have been made in cancer therapies to improve clinical outcomes over last few years. However, therapeutic resistance has always been a major difficulty in cancer therapy, with extremely complicated mechanisms remain elusive. N6-methyladenosine (m6A) RNA modification, a hotspot in epigenetics, has gained growing attention as a potential determinant of therapeutic resistance. As the most prevalent RNA modification, m6A is involved in every links of RNA metabolism, including RNA splicing, nuclear export, translation and stability. Three kinds of regulators, methyltransferase (writer), demethylase (eraser) and RNA binding proteins (reader), together orchestrate the dynamic and reversible process of m6A modification. Herein, we primarily reviewed the regulatory mechanisms of m6A in therapeutic resistance, including chemotherapy and targeted therapy. Then we discussed the clinical potential of m6A modification to overcome resistance and optimize cancer therapy. Additionally, we proposed prospects of m6A modification for future research.

Objective SERPINE1 is associated with poor prognosis of many cancers and plays an important role in tumor metastasis. This study aims to clarify the specific regulatory mechanism of miR-532-3p/SERPINE1 in colon adenocarcinoma. Methods TCGA database was used to screen differentially expressed mRNAs, and then mirDIP and miRWalk databases were used to analyze and identify upstream regulatory gene miRNAs. GSEA database was used to the analysis of enrichment pathways. Real time quantitative polymerase chain reaction (qRT-PCR), CCK-8, cloning experiment, scratch healing, Transwell, Western blot (WB) to study the regulatory mechanism of SERPINE1 and its upstream genes on proliferation, migration and invasion of colon adenocarcinoma. Results SERPINE1 was significantly overexpressed in colon adenocarcinoma cells and tissues, while miR-532-3p was significantly overexpressed. SERPINE1 is related to the poor prognosis of colon adenocarcinoma patients and can promote the proliferation, migration and invasion of colon adenocarcinoma cells. SERPINE1 was significantly enriched in ECM RECEPTOR INTERACTION pathway. MiR-532-3p targets and negatively regulates the expression of SERPINE1. The reversion experiment shows that miR-532-3p/SERPINE1 regulates the ECM RECEPTOR INTERACTION pathway and affects the malignant progression of colon adenocarcinoma cells. Conclusion As the upstream regulatory gene of SERPINE1, miR-532-3p inhibits the proliferation, migration and invasion of colon adenocarcinoma cells by regulating ECM RECEPTOR INTERACTION. MiR-532-3p/SERPINE1 has the potential to become a new target for the treatment of colon adenocarcinoma.

With the continuous innovation and scientific and technological advances and the deepening of scientific research, the content of transfusion medicine is being constantly updated. This article provides a brief overview of the research progress in transfusion medicine from 2021 to 2022, including blood products uses, cross-disciplinary research and application of cutting-edge technologies, and research related to clinical transfusion and treatment, to provide a reference for discipline construction and development of transfusion medicine in China.

Objective To explore the effect of S100A1 on the proliferation of human thyroid cancer SW579 cells and its mechanism. Methods The human thyroid cancer data sets GSE50901 and GSE138198 were selected, and R software was used to screen the differentially expressed genes in thyroid cancer tissues and normal thyroid tissues. The differentially expressed genes were verified with TGCA database. CCK-8 experiment was used to detect the effect of S100A1 knockdown or overexpression on the proliferation of human thyroid cancer SW579 cell. Western Blot was used to detect the effect of S100A1 on the WNT/β-catenin signaling pathway. Results A joint analysis of the data sets GSE50901 and GSE138198 showed that 97 genes were up-regulated in both data sets, and 46 genes were down-regulated. S100A1 gene is highly expressed in thyroid cancer. Knockdown of S100A1 could inhibit the proliferation of SW579 cells, and overexpression of S100A1 could promote the proliferation of SW579 cells. GSEA analysis found that WNT signal pathway was significantly enriched after knocking down S100A1 in SW579 cells, and the signal pathway activity was reduced. Western Blot results showed that the protein expression levels of β-catenin, c-myc and cyclin D1 in the siS100A1 group were significantly lower than those in the siNeg group, while the protein expression levels of β-catenin, c-myc and cyclin D1 in the S100A1 group were significant higher than those in the EGFP group. Conclusion S100A1 is highly expressed in thyroid cancer. Knockdown of S100A1 might inhibit the proliferation of thyroid cancer SW579 cells by inhibiting the activity of WNT/β-catenin signaling pathway.

Platelets play a crucial role in a variety of physiologic and pathologic processes, especially in hemostasis and wound healing. In recent years platelet-rich plasma, platelet-rich fibrin, platelet-lysate and other platelet-derived products have become a promising treatment in regenerative medicine and have been widely applied clinically. By release a variety of growth factors, cytokines, and chemokines, platelet-derived products induce cell migration, proliferation, differentiation, and chemotaxis, stimulating mitosis in multiple cell types and neovascularization, increasing endothelial cell response to pro-angiogenic factors, and promoting fibroblast migration and proliferation. This article reviews the classification and origin of platelet-derived products, biological characteristics of the main growth factors, and their therapeutic effects in promoting the healing of various wounds, then, also analyzed the possible issues and the future development possibilities.