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.

Abnormal DNA methylation of tumor suppressor gene promoter has been found in breast cancer. Therefore, the current study set out to explore how DNA methyltransferase 1 (DNMT1) affects breast cancer through mediating miR-497/GPRC5A axis.

DNA methyltransferase 1 inhibits microRNA-497 and elevates GPRC5A expression to promote chemotherapy resistance and metastasis in breast cancer.

Histidine triad nucleotide‑binding protein (HINT) belongs to the histidine triad protein family. Recent studies have demonstrated that HINT1 and HINT2 both play a pivotal role in cancer growth. However, the functions of HINT3 in various types of cancer, including breast cancer (BRCA), have not yet been fully elucidated. In the present study, the role of HINT3 in BRCA was investigated. Based on The Cancer Genome Atlas and reverse transcription‑quantitative PCR analyses, HINT3 was found to be decreased in BRCA tissues. , HINT3 knockdown promoted the proliferation and colony formation of, and 5‑ethynyl‑2'‑deoxyuridine incorporation in MCF‑7 and MDA‑MB‑231 BRCA cells. By contrast, HINT3 overexpression suppressed DNA synthesis and the proliferation of both cell lines. Apoptosis was also found to be modulated by HINT3. , HINT3 ectopic expression attenuated the tumorigenesis of MDA‑MB‑231 and MCF‑7 cells in a mouse tumor xenograft model. Furthermore, HINT3 silencing or overexpression also enhanced or inhibited, respectively, the migratory capacity of the MCF‑7 and MDA‑MB‑231 cells. Finally, HINT3 upregulated phosphatase and tensin homolog (PTEN) at the transcriptional level, which resulted in the inactivation of AKT/mammalian target of rapamycin (mTOR) signaling both  and . Taken together, the present study demonstrates that HINT3 inhibits the activation of the PTEN/AKT/mTOR signaling pathway, and suppresses the proliferation, growth, migration and tumor development of MCF‑7 and MDA‑MB‑231 BRCA cells.

HINT3 suppresses AKT/mTOR signaling pathway activity during breast cancer tumorigenesis through PTEN transcriptional activation.

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
DNA methyltransferase 1 inhibits microRNA-497 and elevates GPRC5A expression to promote chemotherapy resistance and metastasis in breast cancer. Cancer cell international\| PubMed ID: 35255904	2022
HINT3 suppresses AKT/mTOR signaling pathway activity during breast cancer tumorigenesis through PTEN transcriptional activation. International journal of molecular medicine\| PubMed ID: 37203409	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

Dahai Chai

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