Research Progress on the Protective Effect of Intestinal Flora on Radiation-induced Lung Injury in Thoracic Tumors / 中国肺癌杂志

Radiation therapy is one of the main treatment methods for patients with thoracic malignant tumors, which can effectively improve the survival rate of the patients. However, radiation therapy can also cause damage to normal tissues while treating tumors, leading to radiation-induced lung injury such as radiation pneumonia and pulmonary fibrosis. Radiation-induced lung injury is a complex pathophysiological process involving many factors, and its prevention and treatment is one of the difficult problems in the field of radiation medicine. Therefore, the search for sensitive predictors of radiation-induced lung injury can guide clinical radiotherapy and reduce the incidence of radiation-induced lung injury. With the in-depth study of intestinal flora, it can drive immune cells or metabolites to reach lung tissue through the circulatory system to play a role, and participate in the occurrence, development and treatment of lung diseases. At present, there are few studies on intestinal flora and radiation-induced lung injury. Therefore, this paper will comprehensively elaborate the interaction between intestinal flora and radiation-induced lung injury, so as to provide a new direction and strategy for studying the protective effect of intestinal flora on radiation-induced lung injury.
.

Research progress on the radiotherapy treatment of brain metastases from non-small cell lung cancer / 中华放射肿瘤学杂志

The incidence rate of lung cancer ranks second and the mortality rate ranks first in the world. Non-small cell lung cancer (NSCLC) is the main pathological type and is prone to brain metastasis. At present, the main treatment methods of brain metastases from NSCLC include surgery, radiotherapy, chemotherapy, molecular targeting and immunotherapy. Radiotherapy is a common local treatment of brain metastases. With the development of technology and drugs, how to combine radiotherapy with other treatments is a hot topic in clinical research. In this article, advances in radiotherapy for brain metastases from NSCLC were reviewed, aiming to provide reference for the selection of treatment options in clinical practice.

Practice and exploration of online teaching of oncological radiotherapy during standardized residency training / 中华医学教育探索杂志

This study takes the online teaching of oncological radiotherapy for standardized residency training in Harbin Medical University Cancer Hospital as an example, interprets the practice of carrying out online education, thinks about the problems in the teaching process, and is committed to making great contributions to the improvement of medical education quality in the new era and new background.

Mechanism and Research Progress of Microbiome in the Development of Lung Cancer / 中国肺癌杂志

Lung cancer is one of the most common malignant tumors with poor prognosis in China, and most patients are diagnosed as advanced patients. Studies have shown that the microecological characteristics of lung cancer patients are different from healthy people, and the microorganisms of the respiratory tract can affect the occurrence and development of lung cancer through various mechanisms. In recent years, the study of the correlation between microbiome and disease has become another research hotspot following the Human Genome Project. However, at present, there are relatively few studies on the characteristics of lung cancer and respiratory microbiome. Therefore, it is necessary to further explore the potential relationship between lung cancer and microbial flora. By studying the mechanism of action of respiratory microorganisms in the development of lung cancer, it is expected to provide a clearer scientific basis in the clinical diagnosis, treatment and prognosis assessment of lung cancer. This article reviews the current researches on microbial flora and lung cancer, and provides new ideas for clinical diagnosis and treatment of lung cancer.
.

Metabolic reprogramming orchestrates CD4+ T-cell immunological status and restores cardiac dysfunction in autoimmune induced-dilated cardiomyopathy mice.

Cellular autoimmune responses, especially those mediated by T-cells, play vital roles in the immunopathogenesis of dilated cardiomyopathy (DCM). Metabolic reprogramming directly controls T-cell function, imprinting distinct functional fates. However, its contribution to T-cell dysfunction and the immunopathogenesis of DCM is unknown. Here, we found that in DCM patients, CD4+ T-cells exhibited immune dysfunction and glycolytic metabolic reprogramming based on extracellular acidification and oxygen consumption rates. Similar results were observed in splenic and cardiac CD4+ T-cells from autoimmune-induced DCM mice. In vitro, the glycolysis inhibitor 2-deoxy-d-glucose (2-DG) reversed T-cell dysfunction; thus, heightened metabolic activity directly controls CD4+ T-cell immunological status. Adoptive transfer of CD4+ T-cells from DCM mice to normal recipients induced cardiac remodeling and cardiac T-cell dysfunction. Strikingly, these effects were abolished by preconditioning cells with 2-DG, indicating that CD4+ T-cell dysfunction partially induced by metabolic reprogramming contributes to cardiac remodeling. Moreover, the microRNA let-7i modulated the metabolism and function of T-cells from DCM mice by directly targeting Myc. Collectively, our results show that metabolic reprogramming occurs in T-cells of autoimmune-induced DCM mice and patients. Further, our findings highlight that glycolytic metabolism is a critical contributor to T-cell dysfunction and DCM immunopathogenesis. Our data position the modulation of the metabolism as a central integrator for T-cell function, representing a promising strategy against autoimmune-mediated DCM progression.

CircVRK1 regulates tumor progression and radioresistance in esophageal squamous cell carcinoma by regulating miR-624-3p/PTEN/PI3K/AKT signaling pathway.

As a novel class of noncoding RNAs (ncRNAs), circular RNAs (circRNAs) have been verified to be potential biomarkers and therapeutic targets for human malignant tumors. However, the thorough understanding of circRNAs in the progression of esophageal squamous cell carcinoma (ESCC) still needs to be improved. This study focused on exploring the function and mechanism of circVRK1 in ESCC. At first, we examined the expression level of circVRK1 in ESCC tissues and cell lines with qRT-PCR. We found that circVRK1 was downregulated in ESCC tissues and cell lines. Kaplan-Meier method was used to analyze the correlation between circVRK1 expression and the overall survival of ESCC patients. Functionally, overexpression of circVRK1 suppressed the cell proliferation, migration and epithelial-mesenchymal transition (EMT) and reversed the radioresistance. Therefore, we identified the tumor suppressive role of circVRK1 in ESCC progression. Mechanistically, circVRK1 positively regulated PTEN by acting as a molecular sponge of miR-624-3p. Moreover, circVRK1 decreased the activity of PI3K/AKT signaling pathway by upregulating PTEN. Rescue assays were carried out to confirm the function of circVRK1-miR-624-3p-PTEN axis in ESCC progression. Our findings showed that circVRK1 suppressed ESCC progression by regulating miR-624-3p/PTEN axis and PI3K/AKT signaling pathway, suggesting the potential therapeutic value of circVRK1 for ESCC.

Slug Is Associated With Tumor Metastasis and Angiogenesis in Ovarian Cancer.

Ovarian cancer is the most lethal gynecologic malignancy among women and usually initiated by the malignant transformation of epithelial cells. The progression of ovarian cancer involves a cascade of events, including tumor cell epithelial-mesenchymal transition (EMT), invasion, migration, and angiogenesis. Slug plays vital roles in the development of motile and invasive manner of cancer cells via EMT progression. The present work is devoted to investigate the effect of slug on the invasion and angiogenesis in ovarian cancer. The findings reveal that tumors with high expression of slug (44 of 60) represent higher tumor grade, lymph node metastasis, and worse prognosis than those with low expression (16 of 60; P < .05). We also identified a significant correlation between the slug and the microvessel density (MVD). Results of transwell migration assay showed that decreased slug induced by short hairpin RNA contributed to the repressed invasion and migration of SKOV3 cells. Additionally, the migration and tube formation capacity of human umbilical vein endothelial cells were markedly decreased in SKOV3-sh-conditioned medium compared to SKOV3 and SKOV3-NC. Furthermore, xenograft mouse models (SKOV3/SKOV3-sh cells injection into BALB/c nude mice) were developed to validate the effects of slug. The data confirmed that inhibited expression of slug extensively decreased the growth of tumor and MVD in vivo. Moreover, knockdown of slug can significantly reduce tumor angiogenesis of SKOV3 cells via ccn1/vascular endothelial growth factor. Thus, our present study demonstrates that slug is closely associated with tumor metastasis and angiogenesis in ovarian cancer.

Protosappanin A increases the sensitivity of gastric cancer SGC-7901 cells to radiotherapy / 实用肿瘤学杂志

Objective In this study,Protosappanin A,Caesalpinia Sappan L extract and Cisplatin were combined with radiotherapy in gastric cancer cell SGC-7901 to investigate whether the Protosappanin A could in-crease radiosensitivity( SER) in gastric cancer SGC-7901 cells. This will be medication to create new areas of in-novation in the future. Methods The cell proliferation of SGC-7901 cells was detected by MTT assay. The rela-tionship between the effect of the Protosappanin A on cell proliferation and the time of action was determined. Caesalpinia Sappan L extract and Cisplatin were as controls. The fitted cell survival curve and clonal formation as-says were used to determine the SER to analyze the sensitizative effect of Protosappanin A. Results Protosappa-nin A could inhibit the growth of SGC-7901 cells,and its inhibitory effect is relatively weak. Its cytotoxicity has a time-and concentration-dependent manner. Cellular morphological changes were observed accompanying with increased concentrations and time treatments of Protosappanin A. Clonal formation experiment showed that the Protosappanin A significantly increased the radiosensitivity of SGC-7901 cells when compared to the radioactive group. They showed a statistically difference. Conclusion The inhibitory effect of the Protosappanin A on SGC-7901 cells in a concentration and time-dependent manner. Protosappanin A combined radiotherapy can improve the radiosensitization of cells,both of which may have synergistic anti-tumor effect.

Expression of TGFbeta1 in pulmonary vein stenosis after radiofrequency ablation in chronic atrial fibrillation of dogs.

The development of pulmonary vein stenosis has recently been described after radiofrequency ablation (RF) to treat atrial fibrillation (AF). The purpose of this study was to examine expression of TGFbeta1 in pulmonary vein stenosis after radiofrequency ablation in chronic atrial fibrillation of dogs. About 28 mongrel dogs were randomly assigned to the sham-operated group (n = 7), the AF group (n = 7), AF + RF group (n = 7), and RF group (n = 7). In AF or AF + RF groups, dogs underwent chronic pulmonary vein (PV) pacing to induce sustained AF. RF application was applied around the PVs until electrical activity was eliminated. Histological assessment of pulmonary veins was performed using hematoxylin and eosin staining; TGFbeta1 gene expression in pulmonary veins was examined by RT-PCR analysis; expression of TGFbeta1 protein in pulmonary veins was assessed by Western blot analysis. Rapid pacing from the left superior pulmonary vein (LSPV) induced sustained AF in AF group and AF + RF group. Pulmonary vein ablation terminated the chronic atrial fibrillation in dogs. Histological examination revealed necrotic tissues in various stages of collagen replacement, intimal thickening, and cartilaginous metaplasia with chondroblasts and chondroclasts. Compared with sham-operated and AF group, TGFbeta1 gene and protein expressions was increased in AF + RF or RF groups. It was concluded that TGFbeta1 might be associated with pulmonary vein stenosis after radiofrequency ablation in chronic atrial fibrillation of dogs.

Effects of pyrrolidine dithiocarbamate on antioxidant enzymes in cardiomyopathy induced by adriamycin in rats.

OBJECTIVE: The clinical usefulness of adriamycin (ADR) is restricted by the frequent induction of dose-dependent chronic cardiomyopathy. Previous studies on ADR cardiotoxicity have reported that the formation of free reactive oxygen radicals might be involved in ADR cardiotoxicity. Pyrrolidine dithiocarbamate (PDTC) is a potent antioxidant in vivo and in vitro. The present study was undertaken to examine the effects of PDTC on antioxidant enzymes in cardiomyopathy induced by ADR in rats. METHODS: Thirty-two male Wistar rats were randomly divided into 4 groups: control, ADR, PDTC, and ADR+PDTC. After 30 days, myocardial histopathological and electron microscopic examinations were performed: the myocardial content of superoxide anion and lipid peroxides were examined; the myocardial total antioxygenation capability (T-AOC) and activity of glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) were examined; myocardial GSH-Px, Mn-SOD and Cu,Zn-SOD gene expressions were examined by RT-PCR analysis, and the myocardial expression of GSH-Px, Mn-SOD and Cu,Zn-SOD proteins was assessed by Western blot analysis. RESULTS: At 30 days, ADR-induced cardiomyopathy was confirmed by structural examination. The changes were prevented by PDTC. Myocardial superoxide anion and lipid peroxides were increased by ADR, and these changes were also inhibited by PDTC. ADR decreased myocardial T-AOC and the activity of GSH-Px and SOD, and these changes were likewise inhibited by PDTC. mRNA and protein expression of GSH-Px and Mn-SOD were depressed by ADR treatment and prevented by PDTC. Cu,Zn-SOD mRNA and protein levels were not significantly changed by ADR or PDTC. CONCLUSION: PDTC prevented ADR cardiomyopathy in rats by upregulating GSH-Px and SOD activation, which is associated with changes in the expression of GSH-Px and Mn-SOD transcript and protein levels.