Background: Breast cancer (BC) remains a prevalent and common form of cancer with high heterogeneity. Making efforts to explore novel molecular biomarkers and serve as potential disease indicators, which is essential to effectively enhance the prognosis and individualized treatment of BC. FBXO proteins act as the core component of E3 ubiquitin ligase, which play essential regulators roles in multiple cellular processes. Recently, research has indicated that FBXOs also play significant roles in cancer development. However, the molecular functions of these family members in BC have not been fully elucidated.Methods: In this research, we investigated the expression data, survival relevance and mutation situation of 10 FBXO members (FBXO1, 2, 5, 6, 16, 17, 22, 28, 31 and 45) in patients with BC from the Oncomine, GEPIA, HPA, Kaplan–Meier Plotter, UALCAN and cBioPortal databases. The high transcriptional levels of FBXO1 in different subtypes of BC were verified by immunohistochemical staining and the specific mutations of FBXO1 were obtained from COSMIC database. Top 10 genes with the highest correlation to FBXO1 were identified through cBioPortal and COXPRESdb tools. Additionally, functional enrichment analysis, PPI network and survival relevance of FBXO1 and co-expressed genes in BC were obtained from DAVID, STRING, UCSC Xena, GEPIA, bc-GenExMiner and Kaplan–Meier Plotter databases. FBXO1 siRNAs were transfected into MCF-7 and MDA-MB-231 cell lines. Expression of FBXO1 in BC cell lines was detected by western-blot and RT-qPCR. Cell proliferation was detected by using CCK-8 kit and colony formation assay. Cell migration was detected by wound‐healing and transwell migration assay.Results: We found that FBXO2, FBXO6, FBXO16 and FBXO17 were potential favorable prognostic factors for BC. FBXO1, FBXO5, FBXO22, FBXO28, FBXO31 and FBXO45 may be the independent poor prognostic factors for BC. All of them were correlated to clinicopathological staging. Moreover, knockdown of FBXO1 in MCF7 and MDA-MB-231 cell lines resulted in decreased cell proliferation and migration in vitro. We identified that FBXO1 was an excellent molecular biomarker and therapeutic target for different molecular typing of BC.Conclusion: This study implies that FBXO1, FBXO2, FBXO5, FBXO6, FBXO16, FBXO17, FBXO22, FBXO28, FBXO31 and FBXO45 genes are potential clinical targets and prognostic biomarkers for patients with different molecular typing of BC. In addition, the overexpression of FBXO1 is always found in breast cancer and predicts disadvantageous prognosis, implicating it could as an appealing therapeutic target for breast cancer patients.

The malignant phyllodes tumor (PT) of the breasts is a rare type of fibroepithelial neoplasm. Osteoclast-like giant cells (OLGCs) exist in many types of tumors. But malignant PTs with OLGCs were rarely reported. Here, we presented a case of a 49-year-old woman who had a 23 cm ×21 cm ×6 cm mass which was growing for 2 years in her left breast. The patient had moderate anemia due to the hemorrhage and exudation on the surface of the tumor. The imaging examinations such as PET-CT found no lymphatic involvement and distant metastasis. We performed mastectomy with a 2 cm surgical margin and free skin flap transplantation to restore the big wound. The vacuum assisted closure (VAC) system was used to promote wound healing. Histological examination of the surgical specimen showed atypical spindle-like stroma cells, marked nuclear pleomorphism, focal necrosis, and mitotic activity. Typical leaf-like architectures of PTs were observed in some regions. OLGCs were found in many sections of the tumor with a number of vascular proliferations. The final diagnosis was malignant PT with OLGCs. After a three-month follow-up, no local recurrence or metastasis was found. Autogenous skin grafts with VAC are available for large area skin defect after excising a huge breast tumor. The presence of OLGCs in malignant tumors may be related to necrosis and hemorrhage of the tumor. These findings also provide opportunities for understanding the mechanisms of tumor formation and development.

Globally, breast cancer is the most common malignancy among women and thyroid cancer is also one of the common cancer types among women. Patients with breast cancer exhibit a higher incidence of thyroid cancer than that noted in the general population. The exact mechanism of multiple tumors remains elusive. In the present study, the case of a patient with multiple tumors harboring gene mutation is reported. Specifically, a patient with lymphoepithelioma‑like carcinoma of the breast (LELC‑B) and thyroid cancer is described. It was hypothesized that the short interval between the onset of these two types of malignant tumor may be related to the TP53 gene mutation status of the patient. To date, a specific relationship between gene mutations and multiple tumors is yet to be determined. Therefore, additional studies are required to address this topic.

Objective: The immune status of the tumor microenvironment significantly impacts the clinical prognosis of triple-negative breast cancer (TNBC). The involvement of long noncoding RNAs (lncRNAs) in tumor immune infiltration is widely acknowledged. Therefore, it is crucial to explore the role of significant immune-related lncRNAs in TNBC. Methods: We acquired RNA, single-cell sequencing, and clinical information on TNBC from The Cancer Genome Atlas (TCGA) and the Gene Expression Omnibus (GEO) databases. To identify immune-related lncRNAs, immune infiltration subgroups were determined and verified using single-sample gene-set enrichment analysis, non-negative matrix factorization, and weighted gene co-expression network analysis. CIBERSORTx, deconvolution, drug sensitivity, and Scissor analyses revealed that differences in cell type and drug efficacy were associated with immune grouping. Results: TNBC samples were classified into immune-desert (cold) and immune-inflamed (hot) subgroups based on a lncRNA model (including LINC01550, LY86-AS1, LINC00494, LINC00877, CHRM3-AS2, HCP5, MIR155HG, and PIK3CD-AS1). Furthermore, using in vitro experiments, we found that LINC01550 promoted malignant phenotypes, including proliferation, survival, and migration of TNBC. The immune-inflamed subgroup exhibited significantly lower half-maximal inhibitory concentration values for common anti-tumor drugs, including palbociclib, ribociclib, mitoxantrone, and sorafenib (T-test, P < 0.001). This may be related to the fact that the immune-inflamed subgroup has more plasmacytoid dendritic cells (pDCs) and B cells than those in immune-desert subgroups (P < 0.001). Conclusions: Differences in specific cell infiltration can lead to increased sensitivity of the immune-inflamed subgroup to anti-tumor drugs. The proposed lncRNA model holds great promise to assess the immune landscapes and therapeutic reactions of TNBC patients.

Breast cancer progression is closely associated with metabolic imbalance, particularly lipid metabolic reprogramming, which supports tumour growth. This study investigated the expression of CYP4Z1, a member of the cytochrome P450 family, in breast cancer cells and its role in tumour progression. CYP4Z1 was markedly overexpressed in breast cancer tissues and strongly associated with poor patient prognosis. Functional experiments revealed that CYP4Z1 silencing inhibited proliferation, migration and epithelial–mesenchymal transition while promoting apoptosis and senescence in breast cancer cells; in contrast, CYP4Z1 overexpression enhanced malignant behaviour. Nontargeted lipidomics revealed that CYP4Z1 downregulation disrupted lipid homeostasis, particularly by inducing triglyceride accumulation, suggesting its importance in maintaining tumour lipid metabolism. Mechanistically, bioinformatics analysis and dual-luciferase assays confirmed that FOXA1 represses CYP4Z1 promoter activity. The loss of FOXA1 activated CYP4Z1, triggered lipid metabolic reprogramming and promoted malignant phenotypes. Rescue experiments further demonstrated that CYP4Z1 silencing reversed the proliferation, migration and abnormal lipid accumulation induced by FOXA1 deficiency. Overall, these findings suggest that CYP4Z1 may contribute to breast cancer progression in association with lipid metabolic remodelling and support the involvement of the FOXA1–CYP4Z1 axis in this process. This axis may represent a candidate mechanism warranting further investigation in translational studies.