A bibliometric and visualization analysis of research trends and hotspots on targeted therapy for breast cancer from 2003 to 2022.

Background: Breast cancer is a significant public health issue, exhibiting the most pronounced occurrence and fatality rates among malignant neoplasms globally. Targeted therapy is a medical intervention that focuses on specific molecular markers. This study aims to investigate and evaluate the current research trends and directions in the field of targeted therapy for breast cancer using bibliometric analysis. Method: The Web of Science database was utilized to retrieve relevant articles published between 2003 and 2022. The VOSviewer software and Bibliometrix package in the R language were employed to conduct co-occurrence and clustering analyses of authors, countries, institutions, journals, references, and the CiteSpace tool was utilized for keyword burst detection. Results: A total of 2,258 articles were included and the annual number of publications increased rapidly. The most prolific country on this topic was the USA (n=898, 39.77%) and the University of Texas MD Anderson Cancer Center published most papers (n=93). Dennis J. Slamon and Gabriel N. Hortobagyi stood out in the field, with Dennis J. Slamon leading in terms of co-citations(n=653) and Gabriel N. Hortobagyi topping the list in terms of published articles(n=18). The most productive journal was Breast Cancer Research and Treatment and the most cited journal was Journal of Clinical Oncology. The clustering of keywords indicated that the primary focus of researches in the past two decades was on the development and clinical evaluation of tumor-targeted drugs associated with the epidermal growth factor receptor (EGFR) family signaling pathway, and explored mechanisms related to biological behavior of breast cancer. Keywords co-occurrence and burst analysis identified current research hotspots and potential research trends. Conclusion: This study employed bibliometric analysis to examine research on targeted therapy for breast cancer over a span of 20 years, and identified development trends of research and elucidated potential research trajectories in the domain of this topic. This study helps in the identification of prospective collaborators and partner institutions for researchers.

HMGB3 Targeted by miR-145-5p Impacts Proliferation, Migration, Invasion, and Apoptosis of Breast Cancer Cells.

This study focused on the investigation into how HMGB3 works in breast cancer (BC) progression. Firstly, we analyzed the relationship between HMGB3 and BC patients through the TCGA database. We performed qRT-PCR for determining the HMGB3 mRNA level and Western blot for detecting the protein level of HMGB3 in BC cell lines. CCK-8, flow cytometry, transwell, and wound healing assays were utilized to detect the effect of HMGB3 on BC cell phenotypes. Next, the prediction of the binding site shared by miR-145-5p and HMGB3 was performed by the bioinformatics method. The targeting relationship between miR-145-5p and HMGB3 was validated by using dual-luciferase assay. Finally, rescue experiments were employed for assessing the effect of the miR-145-5p/HMGB3 axis on BC cells. HMGB3 was demonstrated to have a high-level expression in BC cell lines and facilitated BC progression. On the contrary, miR-145-5p was shown a low-level expression in BC cell lines, which could target HMGB3. miR-145-5p restrained the proliferation, migration, and invasion of BC cells via inhibiting HMGB3.

Research on the effect of interfering with miRNA-155 on triple-negative breast cancer cells.

BACKGROUND: Triple negative breast cancer (TNBC) is a poor prognosis breast cancer with the highest mutation rate and limited treatment options. MiR-155 is highly expressed in TNBC, but its role and potential mechanism in TNBC remain to be elucidated. OBJECTIVE: The aim of this study is to examine the effect of interfering with miRNA-155 on the inflammatory pathway of NLRP 3 in TNBC (MDA-MB-231). METHODS: MiRNA-155-specific interference (Si-miR-155) on MDA-MB-231 cell was manifested by transfection of miRNA-155 inhibitor. Meanwhile, blank control (Blank) and negative control (NC) were set. Cell growth and proliferation rate were detected by MTT; apoptosis rate were detected by flow cytometry; colony forming test was used to detected cell viability; cell migration ability was detected by Wound healing assay; TNF-α, IL-18, IL-6 and IL-1ß levels were detected by ELISA. The mRNA of miRNA-155, NLRP3, ASC, caspase-1 and Ki67 were detected by qRT-PCR. The expression levels of NLRP3, caspase-1, ASC and Ki67 were detected by Western blotting. RESULTS: The proliferation rate of Si-miRNA-155 group decreased, while the apoptosis rate increased significantly. After interfering with miRNA-155, the number of cancer cell colonies and the migration ability was decreased, and the secretion levels of IL-18, TNF-α, IL-6 and IL-1ß were also inhibited. Moreover the mRNA and protein expression of NLRP3, caspase-1, ASC and Ki67 were significantly suppressed. CONCLUSIONS: Interference with miRNA-155 can inhibit the NLRP3 pathway of MDA-MB-231 cells, as well as the proliferation, migration and inflammatory factor secretion of MDA-MB-231 cell, and can accelerate its apoptosis.