Recently, emerging evidence has suggested that carcinoma-associated fibroblasts (CAFs) could contribute to chemotherapy resistances in breast cancer treatment. The aim of this study is to compare the gene expression profiling of CAFs before and after chemotherapy and pick up candidate genes that might associate with chemotherapy resistance and could be used as predictors of treatment response. CAFs were cultured from surgically resected primary breast cancers and identified with immunohistochemistry (IHC) and Flow cytometry (FCM). MDA-MB-231 cells were cultured as the breast cancer cell line. Cell adhesion assay, invasion assay, and proliferation assay (MTT) were performed to compare the function of MDA-MB-231 cells co-cultured with CAFs and MDA-MB-231 cells without co-culture, after chemotherapy. Totally 6 pairs of CAFs were prepared for microarray analysis. Each pair of CAFs were obtained from the same patient and classified into two groups. One group was treated with Taxotere (regarded as after chemotherapy) while the other group was not processed with Taxotere (regarded as before chemotherapy). According to our study, the primary-cultured CAFs exhibited characteristic phenotype. After chemotherapy, MDA-MB-231 cells co-cultured with CAFs displayed increasing adhesion, invasiveness and proliferation abilities, compared with MDA-MB-231 cells without CAFs. Moreover, 35 differentially expressed genes (absolute fold change >2) were identified between CAFs after chemotherapy and before chemotherapy, including 17 up-regulated genes and 18 down-regulated genes. CXCL2, MMP1, IL8, RARRES1, FGF1, and CXCR7 were picked up as the candidate markers, of which the differential expression in CAFs before and after chemotherapy was confirmed. The results indicate the changes of gene expression in CAFs induced by Taxotere treatment and propose the candidate markers that possibly associate with chemotherapy resistance in breast cancer.

Objective: To investigate whether intraoperative neuromonitoring (IONM) has a significant advantage in reducing the incidence of recurrent laryngeal nerve (RLN) injury. Methods: Patients who underwent thyroid and parathyroid surgery from October 2012 to December 2017 at the Center for Thyroid and Breast Surgery of Xuanwu Hospital were retrospectively analyzed. They were divided into the IONM group and visualization alone group (VA group) according to whether IONM was used. Results: In total, 1696 nerves at risk of injury (IONM group, n = 1104; VA group, n = 592) were included in the analysis. Among the high-risk nerves, permanent damage occurred in no cases in the IONM group but in one case in the VA group. Because the higher proportion of central lymph node metastasis caused difficulties in central cervical lymph node dissection and identification of the RLN, the patients undergoing lateral cervical lymph node dissection in the VA group had a significantly higher risk of postoperative RLN injury (11.76% vs. 0.00%). Conclusion: IONM technology has advantages in protection of the RLN, especially in high-risk nerves and patients with a high proportion of central lymph node metastasis who require central and lateral cervical lymph node dissection.

Chemotherapy is an important comprehensive treatment for breast cancer, which targets micro‑environment of tumors as well as their characterisitcs. A previous microarray analysis revealed that matrix metalloproteinase (MMP)‑1 was highly upregulated in carcinoma-associated fibroblasts (CAFs) prior to and following treatment with Taxotere under co‑culture conditions. However, whether the chemotherapeutic effects of Taxotere were influenced by the changes in MMP‑1 remained unclear. The purpose of the present study was to investigate the impact and mechanism of CAFs in regulating the efficacy of Taxotere on breast cancer cells. CAFs isolated from primary invasive ductal human breast tumors following surgical resection, were used in co‑culture with MDA‑MB‑231 cells to simulate the tumor micro‑environment. Following the addition of Taxotere, changes in MMP‑1 gene and protein expression were assessed by reverse transcription‑quantitative polymerase chain reaction and western blot analysis, respectively. Proliferation, invasion and apoptosis assays revealed that when MMP‑1 was upregulated in CAFs, the therapeutic efficacy of Taxotere was reduced in breast cancer cells. Chemosensitivity was significantly increased when MMP‑1 expression was inhibited by GM6001. In addition, Collagen IV was upregulated in CAFs following chemotherapy and protected breast cancer cells against chemotherapeutic side effects. Collagen IV expression significantly decreased, as well as MMP‑1 expression when GM6001 was added. Proliferation and invasion assays demonstrated that the exogenous addition of Collagen IV weakend the chemotherapeutic effect of Taxotere on breast tumor cells. Overall, the results revealed that in CAFs, MMP‑1 synergized with Collagen IV as a key gene in regulating the chemotherapeutic effect of Taxotere on breast tumor cells and served an important role in reducing the efficacy of Taxotere on breast cancer, potentially via the transforming growth factor‑β signaling pathway. These fidings provide a theoretical basis for the mechanism of CAFs in reducing the chemotherapeutic effect of Taxotere on breast cancer cells and a novel approach for enhancing the chemosensitivity of tumors.