Objective To investigate the expression characteristics of RAB1A in the breast tumor microenvironment (TME) and its mechanism of promoting tumor metastasis, with the aim of identifying potential targets for TME-targeted antimetastatic therapy. Methods Proteomic sequencing was performed on tumor and adjacent tissues from 16 patients with triple-negative breast cancer (TNBC) or HER2-overexpressing breast cancer. Single-cell RNA sequencing was conducted on biopsy samples from four patients with TNBC or HER2-overexpressing breast cancer. TME cell heterogeneity and RAB1A expression patterns were analyzed at the proteomic and single-cell transcriptomic levels. ELISA and wound healing assays were utilized to verify the mechanism by which RAB1A regulates the function of cancer-associated fibroblasts (CAFs), thereby promoting the metastasis of TNBC cells. Results RAB1A was specifically highly expressed in CAFs. Functional module analysis indicated an association with the prometastatic secretion pathway and matrix remodeling modules. Human mammary fibroblasts (HMFs), CAFs, and RAB1A-overexpressing CAFs (CAF-OE-RAB1A) were cocultured with MDA-MB-231 cells for 24 h. The wound healing assay revealed that after 24 h of coculture with MDA-MB-231 cells, the CAF coculture group exhibited a significantly higher migration rate (38.86%) than the negative control (25.07%, P<0.01) and HMF coculture groups (30.56%, P<0.05). Notably, the migration rate in the CAF-OE-RAB1A coculture group further enhanced to 47.21% relative to that in the CAF coculture group (P<0.05). Additionally, TGF-β1 secretion in the CAF-OE-RAB1A coculture group (1030.56 pg/ml) was markedly elevated relative to that in the CAF (417.62 pg/ml, P<0.001) and HMF coculture groups (29.52 pg/ml, P<0.0001). Conclusion RAB1A is specifically highly expressed in CAFs within the breast cancer TME. It may be involved in the metastatic process of breast cancer. Furthermore, RAB1A can promote TNBC cell migration by regulating the secretory function of CAFs.

Triple-negative breast cancer(TNBC)is characterized by tumor heterogeneity and diverse tumor microenvironment(TME),which make its research and treatment more difficult.Chemotherapy is an important TNBC treatment;however,predicting post-treatment effic-acy and chemoresistance remain urgent clinical challenges,with changes in the TME being a major cause.Understanding the facilitating role of the TME is crucial to resolve the challenges.In this study,we assessed the findings of multi-omics studies to explore the research progress on the correlation between the TME and clinical efficacy and chemotherapy resistance of TNBC.We hope to provide a possible direction to improve clinical efficacy and overcome chemotherapy resistance in TNBC.

Objective To discuss the diagnosis and management of tracheomalacia complicating large goiter. Methods Clinical data of 36 patients with large goiter complicated by tracheomalacia at Xijing Hospital between 1992 and 2004 were retrospectively reviewed. Preoperative Valsalva-Mueller test were performed in all patients before undergoing subtotal thyroidectomy with tracheal suspension, and two patients were treated by subtotal thyroidectomy with tracheal suspension and tracheostomy. Results Valsalva-Mueller test was positive in all patients. The compressed tracheal cartilage disappeared in 2 cases, became thin and soft in other 34 cases. Thirty-four patients who underwent subtotal thyroidectomy with tracheal suspension recovered and 2 patients were resued by tracheal suspension with tracheostomy. There was no mortality. Postoperative 34 cases were followed-up from 6 months to 13 years. Thirty-two cases had no postoperative respiratory obstruction, 2 patients died of unrelated diseases. Conclusions The diagnosis of tracheomalacia from large goiter is based on Valsalva-Mueller test and operative detection. Subtotal thyroidectomy with tracheal suspension is the treatment of choice for tracheomalacia complicating large goiter.

0.05). The upper extremity function in group C was better than that in group H (P