Traditional Chinese medicine for breast cancer treatment: a bibliometric and visualization analysis.

CONTEXT: The use of traditional Chinese medicine (TCM) for breast cancer patients inhibits tumor cell growth and proliferation, alleviates adverse reactions, and inhibits tumor recurrence and metastasis post-surgery. An assessment of its historical efficacy and an examination of the latest research trends are imperative to thoroughly leverage the potential of TCM for breast cancer treatment. OBJECTIVE: This study analyzes the published literature on TCM for breast cancer treatment using bibliometric analysis to determine the current state, identify hot spots, and discern trends, providing insight into research in this field. METHODS: TCM-based breast cancer treatment publications between 2003 and 2022 were retrieved from the Web of Science, China National Knowledge Infrastructure, Wanfang, and Duxiu databases. Visual analysis was performed using VOSviewer (V1.6.19) and CiteSpace (V6.3.R1) software. Examined metrics included the annual publication count, literature and journal, national and institutional contributions, author co-occurrence, keyword co-occurrence, keywords timeline, and keywords with citation bursts in this research field. RESULTS AND CONCLUSION: A total of 1080 English publications and 2617 Chinese publications were included in the analysis. China was the leading contributor of publications. High-frequency keywords such as 'apoptosis', 'expression', 'in vivo', 'chemotherapy', 'triple-negative breast cancer', and 'lymphedema' were identified from English and Chinese publications; 'epithelial mesenchymal transition' and 'network pharmacology' emerged as hotspots. The development of modern science, technology, and in-depth research can result in broader prospects for the research and application of TCM in breast cancer treatment, resulting in more effective solutions for the treatment of breast cancer and other malignant tumors.

CircRNA hsa_circ_0070934 functions as a competitive endogenous RNA to regulate HOXB7 expression by sponging miR­1236­3p in cutaneous squamous cell carcinoma.

Circular ribonucleic acids (circRNAs) serve a vital role in the pathological processes of a number of diseases. Previous microarray results of circRNA expression revealed that hsa_circ_0070933 and hsa_circ_0070934, two circRNAs associated with the La ribonucleoprotein 1B gene, were highly expressed in cutaneous squamous cell carcinoma (CSCC). The present study aimed to explore the specific role of these circRNAs in CSCC. Through reverse transcription­quantitative PCR, hsa_circ_0070933 and hsa_circ_0070934 expression levels in CSCC cell lines and a human keratinocyte cell line were detected. Additionally, direct interactions between miR­1236­3p and HOXB7 or circ­0070934 were identified using RNA binding protein immunoprecipitation assays and dual­luciferase reporter assays. Cell Counting Kit­8, 5­ethynyl­2'­deoxyuridine, Transwell invasion and flow cytometry assays were used to assess the roles of miR­1236­3p or circ­0070934 in cell invasion, proliferation and apoptosis. Subsequently, in vivo tumor formation assays were used to verify the role of circ­0070934 in CSCC. The results demonstrated that the expression of circ­0070934 was stably upregulated in a number of CSCC cell lines compared with that in normal human keratinocytes. Knockdown of circ­0070934 inhibited the invasive and proliferative potential of CSCC cells and promoted apoptosis both in vivo and in vitro. In addition, circ­0070934 modulated HOXB7 expression through competitive binding with miR­1236­3p. In conclusion, the results of the present study demonstrated the effects of the circ­0070934/miR­1236­3p/HOXB7 regulatory axis on CSCC and provided a novel insight for the pathogenesis of CSCC.

Circular RNA hsa_circ_0004277 Stimulates Malignant Phenotype of Hepatocellular Carcinoma and Epithelial-Mesenchymal Transition of Peripheral Cells.

Accumulating evidence shows that exosomal circRNAs reflect the physiological status of donor cells, and various cell reactions are induced after exosomal circRNAs are captured by recipient cells. In this study, qRT-PCR was performed to detect circ-0004277 expression in hepatocellular carcinoma (HCC) cell lines, tissues, and plasma exosomes. The effects of circ-0004277 on the proliferation and migration of HCC cells were assessed by cell counting, 5-ethynyl-2'-deoxyuridine assays, Transwell migration assays, and tumor formation in nude mice. We found that circ-0004277 was significantly upregulated in HCC cells, tissues, and plasma exosomes compared to that in normal controls. Overexpression of circ-0004277 enhanced the proliferation, migration, and epithelial-mesenchymal transition (EMT) of HCC cells in vivo and in vitro. Furthermore, exosomes from HCC cells enhanced circ-0004277 expression in surrounding normal cells and stimulated EMT progression. ZO-1, a tight junction adapter protein, was downregulated in HCC tissues. In conclusion, our findings suggest that circ-0004277 promotes the malignant phenotype of HCC cells via inhibition of ZO-1 and promotion of EMT progression. In addition, exosomal circ-0004277 from HCC cells stimulates EMT of peripheral cells through cellular communication to further promote the invasion of HCC into normal surrounding tissues.

PU.1-silenced dendritic cells prolong allograft survival in rats receiving intestinal transplantation.

AIM: To investigate the function of PU.1-silenced semi-mature dendritic cells (DCs) and the possibility of utilizing cell immunity in rat intestinal transplantation. METHODS: DCs were isolated from the bone marrow of F344 rats and cultured using the adherent method. The PU.1 gene was knocked down in DCs using small interfering RNAs (siRNAs) for 24 h, and the cells were then incubated with lipopolysaccharide for 48 h. The PU.1 siRNA that had the highest silencing efficiency was screened using reverse transcription-polymerase chain reaction and Western blot for further study. The tolerance capacity was analyzed and compared between PU.1-silenced DCs (siRNA PU.1 group), negative control-silenced DCs (siRNA NC group) and immature DCs (control group) both in vitro and in vivo. RESULTS: Blocking expression of the PU.1 gene in vitro led to a reduction in DC maturation and an increased tolerance capability. PU.1-silenced DCs expressed moderate levels of major histocompatibility complex (MHC)-II and low levels of co-stimulatory molecules, and produced more interleukin (IL)-10, but less IL-12. Compared with the negative control group, surface molecules cluster of differentiation 80 (CD80), CD86 and MHC-II in the siRNA PU.1 group were 27.0% ± 5.6%, 23.6% ± 4.8% and 36.8% ± 6.8%, respectively, and showed a significantly lower trend (P < 0.05). In vivo treatment of recipients with PU.1-silenced DCs injected before intestinal transplantation (siRNA PU.1 group), significantly prolonged allograft survival and resulted in better tissue histopathology compared with the siRNA NC group and control group. Mean survival time after transplantation was 14.3 ± 3.3 d in the siRNA PU.1 group (P < 0.05). CONCLUSION: PU.1-silenced semi-mature DCs induced partial immune tolerance both in vitro and in vivo, which could be used as a new strategy to promote transplantation tolerance.