Retracted: Long noncoding RNA RHPN1-AS1, induced by KDM5B, is involved in breast cancer via sponging miR-6884-5p.

The above article, published online in Journal of Cellular Biochemistry on 31 January 2020 in Wiley Online Library (https://doi.org/10.1002/jcb.29645), has been retracted by agreement between the authors, the journal's Editor in Chief, Prof. Dr. Christian Behl, and Wiley Periodicals LLC. The authors asked to retract their article after substantial mistakes in experimental data were found, thus the results are considered to be invalid.

Incidence, risk factors, prevention and treatment of postmastectomy pain syndrome in breast cancer: A multicenter study.

BACKGROUND: Postmastectomy pain syndrome (PMPS) is a common postoperative condition after breast cancer surgery. PURPOSE: The aim of this study was to investigate the incidence rate and risk factors of PMPS, and to propose prevention and treatment methods. METHODS: The study included 1790 postoperative breast cancer patients from three hospitals from 2017 to 2021, of which 302 (13.0%) patients with PMPS were included in the study. RESULTS: Age, breast surgery type, axillary surgery type and radiotherapy are the risk factors of PMPS. Age, radiotherapy and chemotherapy affect the pain degree of PMPS during movement. CONCLUSIONS: For breast cancer patients with high risk factors, pain should be actively prevented during perioperative period. Oral pharmacological agents, multidisciplinary combination therapy, local anesthetics and regional anesthesia are the most common treatment of PMPS.

The Prognostic Significance of the Fibrinogen-to-Albumin Ratio in Patients With Triple-Negative Breast Cancer: A Retrospective Study.

Objective: This study aims to investigate the potential prognostic value of fibrinogen-to-albumin ratio (FAR) in patients with triple-negative breast cancer (TNBC). Methods: This study used a retrospective design and enrolled 224 patients with TNBC treated between January 2009 and December 2014 at the Henan Provincial People's Hospital. The receiver operating characteristic curve (ROC) was used to determine the optimal cut-off value for FAR. The associations between TNBC and clinicopathologic categorical variables by FAR were analyzed using the Chi-square test or Fisher's exact test. The survival time and survival curve were determined by Kaplan-Meier survival analysis and compared using the Log-rank method. The potential prognostic factors were determined using univariate and multivariate Cox proportional hazard regression models. Prognostic nomogram was established on the basis of the multivariate analyses. The calibration curves were used to assess the predictive performance. Results: The optimal cut-off value for FAR based on the overall survival (OS) was 0.066, as evaluated by the ROC. The 224 included patients were divided into low FAR group (<0.066) and high FAR group (≥0.066). Univariate and multivariate models shown that FAR was an potential prognostic factor for disease-free survival (DFS) and OS in patients with TNBC. The median DFS and OS of the low FAR group were longer than those of the high FAR group (χ 2 = 15.080, P = 0.0001; χ 2 = 13.140, P = 0.0003), including for pre-menopausal patients, and those with pathological stages I + II, and lymph vessel invasion. A nomogram based on the potential prognostic factors was efficient in predicting 3-, and 5-year DFS and OS survival probabilities. Conclusions: The FAR, which is tested routinely and is characterized by its simplicity, objectivity, and inexpensiveness, is a potential prognostic factor of TNBC, and is potentially applicable in clinical practice.

MiR-140-5p inhibits cell proliferation and metastasis by regulating MUC1 via BCL2A1/MAPK pathway in triple negative breast cancer.

Noncoding RNAs play important roles in the progression of malignant tumors, including triple negative breast cancer (TNBC). Accumulating evidence supported the involvement of the oncogenic MUC1 in tumor metastasis. Our study aimed to explore the roles of miR-140-5p and MUC1 in TNBC and identify the potential underlying mechanisms. In the present study, we found that miR-140-5p expression was significantly decreased in TNBC tissues and associated with advanced clinical features and poor prognosis. MiR-140-5p overexpression suppressed TNBC cells proliferation, invasion ability in vitro and reduced tumor growth in vivo. Subsequently, MUC1 was verified to be a direct target of miR-140-5p in TNBC. Furthermore, we revealed that MUC1 could regulate MAPK pathway through regulating BCL2A1 expression in TNBC. Thus, our study indicated that miR-140-5p might regulate MUC1 to suppress TNBC cells proliferation and metastasis by regulating BCL2A1/MAPK pathway, suggesting miR-140-5p could serve as a potential therapeutic target for TNBC.

HOTAIR may regulate proliferation, apoptosis, migration and invasion of MCF-7 cells through regulating the P53/Akt/JNK signaling pathway.

Breast cancer is a common malignancy, and it is the second leading cause of cancer-related death among women worldwide. The pathogenesis of breast cancer is poorly understood, leading to unsatisfactory efficacy of current anti-PC therapies. The aim of this study is to investigate the role of LncRNA HOTAIR in proliferation, apoptosis, migration and invasion of human breast cancer cell line MCF-7. MCF-7 cells were cultured and transfected with HOTAIR siRNA, and the proliferation rate of cells was determined using MTT and colony-forming assay; moreover, the apoptosis as well as cell cycles were determined using annexin V/propidium iodide staining methods and analyzed using flow cytometery; furthermore, cell scratch and transwell assays have been performed to examine the migration and invasion of MCF-7 cells; Next, cells were collected, and RT-qPCR as well as western blotting assay were performed to examine the expression of P53, MDM2, AKT, JNK, MMP-2 and MMP-9. We discovered that knockdown of HOTAIR induced significant decrease in proliferation and increase in apoptosis of MCF-7 cells, and the cell cycles of HOTAIR siRNA transfected cells have been arrested at G1 phase (p<0.01); moreover, knockdown of HOTAIR lead to marked decrease in the migration and invasion ability of MCF-7 cells; finally, knockdown of HOTAIR induced significant decrease in the expression of P53/Akt/JNK (p<0.01), and significant increase in the expression of P53 in MCF-7 cells (p<0.01). In conclusion, our results proved that HOTAIR may regulate proliferation, apoptosis, migration and invasion of MCF-7 cells through regulating the P53/Akt/JNK signaling pathway.