application-downward-turned-patch-wrapped-prosthesis-method

Application of the Downward-Turned Patch-Wrapped Prosthesis Method in Transaxillary Single-Port Endoscopic Breast Reconstruction

This study presents an innovative breast reconstruction technique using an axillary single-port endoscopic approach with immediate breast reconstruction ...

General Hospital of Ningxia Medical University

Breast cancer (BC) is one of the most common malignant tumors among women worldwide. MicroRNAs (miRs) may be involved in several types of human cancer, including gastric, liver, lung and breast cancer. The aim of the present study was to investigate the effect of miR-1297 on MDA-MB-231 cell epithelial-mesenchymal transition (EMT) and proliferation, and the underlying molecular mechanisms. MDA-MB-231 cells were transfected with miR-1297 inhibitor or inhibitor control for 48 h. Subsequently, MTT and flow cytometry assays indicated that miR-1297 inhibitor significantly decreased cell proliferation and induced apoptosis compared with the inhibitor control group. In addition, reverse transcription-quantitative PCR and western blotting suggested that miR-1297 inhibitor suppressed EMT in MDA-MB-231 cells compared with the inhibitor control group. TargetScan bioinformatics analysis and a dual-luciferase reporter gene assay were performed, which predicted that miR-1297 directly targeted fatty acid 2-hydroxylase (FA2H). Furthermore, MDA-MB-231 cells were transfected with control-plasmid or FA2H-plasmid for 48 h. The results demonstrated that FA2H overexpression decreased MDA-MB-231 cell proliferation and increased apoptosis compared with the control-plasmid group. Additionally, FA2H-plasmid increased E-cadherin expression levels, and reduced N-cadherin and matrix metalloproteinase 9 expression levels at both the protein and mRNA level compared with control-plasmid. Finally, MDA-MB-231 cells were transfected with control-small interfering (si)RNA, FA2H-siRNA, inhibitor control, miR-1297 inhibitor, miR-1297 inhibitor + control siRNA or miR-1297 inhibitor + FA2H-siRNA, and the results suggested that the biological effects of miR-1297 inhibitor were reversed by co-transfection with FA2H siRNA. In conclusion, the present study indicated that miR-1297/FA2H might serve as a novel potential biomarker and therapeutic target for BC.

MicroRNA-1297 downregulation inhibits breast cancer cell epithelial-mesenchymal transition and proliferation in a FA2H-dependent manner.

Opioid binding protein/cell adhesion molecule-like (OPCML) has been demonstrated to be a tumor suppressor gene, as it has been shown in previous studies to play a tumor-suppressive role in a variety of cancers. However, the role of OPCML in breast tumorigenesis remains unclear.

Expression and promoter methylation status of OPCML and its functions in the inhibition of cell proliferation, migration, and invasion in breast cancer.

Potential anti-tumor effects of microRNA-497 (miR-497) have been highlighted in various malignancies including breast cancer. However, little is known about the function of miR-497 and its putative target mucin1 (MUC1) in breast cancer. The present study explored how miR-497 regulates breast cancer progression in a MUC1-dependent manner.

Methylation-Mediated Silencing of MicroRNA-497 Promotes Breast Cancer Progression Through Up-Regulation of Mucin1.

Cancers aggressively reorganize collagen in their microenvironment, leading to the evasion of tumor cells from immune surveillance. However, the biological significance and molecular mechanism of collagen alignment in breast cancer (BC) have not been well established.

HNRNPC promotes collagen fiber alignment and immune evasion in breast cancer via activation of the VIRMA-mediated TFAP2A/DDR1 axis.

Long non-coding RNAs (lncRNAs) are essential in many biological areas like cell growth and apoptosis. The role of recently discovered LINC00702 is yet to be explored. Therefore, we wanted to elucidate its role in breast cancer (BC) with bioinformatic and various methods. LINC00702 expression was predicted using bioinformatic analysis and confirmed by RT-qPCR. Furthermore, the impact of LINC00702 knockdown on BC progression was evaluated. High LINC00702 level could lead to a worse outcome in BC patients. Additionally, CCK-8, EdU,and Annexin V-APC7/AAD experiments showed that LINC00702 knockdown inhibited the growth of BT-474 and T-47D cells and promoted their apoptosis. Moreover, in  experiments showed that shLINC00702-2 significantly reduced tumor sizes and suppressed c-Myc and β-catenin expressions. On the contrary, a rescue assay showed that HLY78, an activator of the Wnt/β-catenin pathway, reversed the cell-inhibiting impact of LINC00702 knockdown. LINC00702 is an oncogenic lncRNA that promotes BC progression by stimulating the Wnt/β-catenin pathway and downstream proteins, making it a promising target for further research on BC treatment.

Knockdown of LINC00702 inhibits the growth and induces apoptosis of breast cancer through the Wnt/β-catenin pathway.

We explored the influence of the TCL6/miR-876-5p axis on breast cancer cell proliferation and migration. Using The Cancer Genome Atlas (TCGA) database, we evaluated the expression of TCL6 in breast cancer patients and studied its effects on cell proliferation, migration, and the cell cycle in vitro. The regulatory effect of miR-876-5p on myosin light chain-2 (MYL2) 3' untranslated regions (3'UTR) was analyzed through luciferase reporter assays, and rescue experiments confirmed TCL6-driven upregulation of MYL2 via a competitive RNA binding mechanism. Furthermore, we used a mouse subcutaneous tumor model to assess the impact of TCL6 knockdown combined with immune checkpoint blockade therapy. Our results indicated that higher TCL6 expression correlated with a favorable prognosis in breast cancer patients. In vitro experiments showed that knockdown of TCL6 and MYL2 enhanced breast cancer cell proliferation and migration. The luciferase and rescue assays demonstrated that TCL6 interacted with miR-876-5p to upregulate MYL2, thereby inhibiting cell proliferation and migration. Both in vitro and in vivo studies revealed that overexpression of TCL6 suppressed tumor growth and improved the response to PD-1 immunotherapy in tumor-bearing mice. This research highlights the pivotal role of lncRNA TCL6 in breast cancer development via a ceRNA network involving miR-876-5p and MYL2, suggesting a novel molecular target for breast cancer therapy.

Article	Year
MicroRNA-1297 downregulation inhibits breast cancer cell epithelial-mesenchymal transition and proliferation in a FA2H-dependent manner. Oncology letters\| PubMed ID: 33014155	2020
Expression and promoter methylation status of OPCML and its functions in the inhibition of cell proliferation, migration, and invasion in breast cancer. Breast cancer (Tokyo, Japan)\| PubMed ID: 33108608	2021
Methylation-Mediated Silencing of MicroRNA-497 Promotes Breast Cancer Progression Through Up-Regulation of Mucin1. Frontiers in oncology\| PubMed ID: 33194611	2020
HNRNPC promotes collagen fiber alignment and immune evasion in breast cancer via activation of the VIRMA-mediated TFAP2A/DDR1 axis. Molecular medicine (Cambridge, Mass.)\| PubMed ID: 37528369	2023
Knockdown of LINC00702 inhibits the growth and induces apoptosis of breast cancer through the Wnt/β-catenin pathway. Heliyon\| PubMed ID: 37860544	2023
LncRNA TCL6 regulates miR-876-5p/MYL2 axis to suppress breast cancer progression. Translational oncology\| PubMed ID: 39874729	2025

Bin Lian

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