<p>Effect of Ect2 Expression on the Growth of Triple-Negative Breast Cancer Cells with Paclitaxel Intervention</p>

Abstract

Object To identify the expression levels of ECT2 (epithelial cell transforming sequence 2) in triple-negative breast cancer (TNBC) before and after administration of paclitaxel (PTX) and explore the interaction between ECT2 and PTX in breast cancer treatment. Methods Lentiviral (LV) packaging ECT2 overexpression and interference plasmids were constructed for in vitro assays. The effects of ECT2 expression on the TNBC cell line (HCC1806), particularly its roles in the proliferation, invasion, migration and apoptosis and cell cycle, were evaluated using the CCK-8 and other methods before and after PTX treatment. In nude mouse xenograft settings were performed to detect cell apoptosis and Ki-67 expression levels by TUNEL and immunohistochemical staining, respectively. Results In the vitro assays, before and after the PTX treatment, comparison of the LV-ECT2 and sh-ECT2 groups and the remaining three groups (control, LV-NC, sh-NC) showed statistically significant differences in terms of cell proliferation, invasion and migration and apoptosis and changes in the cell cycle. In the vivo assays, the control, LV-ECT2 and sh-ECT2 groups markedly outweighed the corresponding PTX-treated groups. The LV-ECT2, PTX, sh-ECT2 and sh-ECT2-PTX were all significantly different from the control group in terms of body weight and tumour size changes. Cell apoptosis occurred in the PTX, sh-ECT2 and sh-ECT2-PTX groups. About the Ki-67 proliferation index, the PTX, LV-ECT2-PTX, sh-ECT2 and sh-ECT2-PTX groups were significantly different from the control group. Conclusion ECT2, which is a major driving factor in the growth of breast cancer cells, plays an important role in regulating TNBC growth. PTX therapy had significantly improved efficacy after silencing ECT2. This finding indicates that the inhibition of ECT2 expression may facilitate the treatment of breast cancer as a new regimen and provide a theoretical basis for the development of new targeted drugs as a replacement for PTX in breast cancer treatment.

Epithelial cell transforming factor ECT2 is an important regulator of DNA double-strand break repair and genome stability

“…As reported by ourselves and others, ECT2 is a potential oncogene that promotes breast tumorigenesis ( 35 , 40 , 41 , 42 , 43 ). Therefore, we wondered if the high expression level of ECT2 found in breast cancer confers cellular resistance to genotoxic insults.…”

Expression and relationship of ECT2 with cell cycle proteins CDK1 and CyclinB1 on the Paclitaxel intervention in three negative breast cancer cells

“…ECT2 promotes the proliferation of tumor cells and mainly acts in the G2/M phase of the cell cycle. In the previous experiments (Wang et al 2020), we established an in vivo and vitro experimental model and carried out PTX treatment, the results showed that the ECT2 overexpression group before and after the PTX treatment the percentage of cell number in the G1 phase and G2/M phase and the change in the DNA content were significantly different from that of the control group, while the ECT2 interference group only had a significant difference in the G2/M phase compared with that of the control group. In this part, we further explored the mechanism of ECT2's effect on the growth and proliferation of TNBC cells by detecting the expression of ECT2 and cell cycle related factors CDK1 and CyclinB1 in the pre-test, and explored the relationship of related indexes after the treatment of PTX, so as to provide a certain theoretical basis for the development of breast cancer and targeted therapy.…”

“…According to the previous experiments (Wang et al 2020), Cell culture is carried out in vitro experiment, the frozen basaloid TNBC cell line HCC1806 (KeyGen Biotech, China) was quickly removed from liquid nitrogen and thawed at 37°C. The cells were then incubated in the medium until the cells grew exponentially, and followed by ECT2 overexpression and interference experiments (interference target sequence: 5ʹ -GCTGAGCATTCCCTTTCCATA-3ʹ).…”

Transcriptomic and Functional Evidence for Differential Effects of MCF-7 Breast Cancer Cell-Secretome on Vascular and Lymphatic Endothelial Cell Growth

“…The genes involved in polo-like kinase 1 (PLK1) pathway and FOXM1 transcription factor network are mostly downregulated, including PLK1, CDC20, AURKA, CCNA2, CCNB2, CDK1, TPX2, PRC1, KIF20A, ECT2, BUB1, and NDC80. The listed genes exhibit oncogenic functions, and thus the inhibition of these genes' expression may contribute to the tumor treatment and provide some basis for the development of new targeted drugs [70][71][72][73][74][75][76][77][78][79].…”