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Breast cancer (BC) has an extremely high global incidence rate. The Xihuang pill (XHP), a traditional Chinese formula, originates from Hongxu Wang's "Life-Saving Manual of Diagnosis and Treatment of External Diseases" written during the Qing Dynasty. In this book, XHP, was first suggested as an anticancer treatment for BC. However, the regulatory mechanism of XHP on BC requires further investigated. To assess the effects of XHP on BC and elucidate the underlying associated signaling network. The influence of XHP on cellular viability, proliferation, and apoptosis of MDA-MB-231 and BT-549 cells were examined. The ability to metastasize was evaluated using Transwell invasion and wound healing tests. Western blotting was used to examine the epithelial-mesenchymal transition (EMT) markers expression. RNA sequencing and bioinformatic analysis were utilized to investigate the regulation mechanism of XHP. A subcutaneous tumor model was developed to study the tumor-inhibitory effects of XHP or/and Doxorubicin (Dox) on BALB/c nude mice, and the EMT marker levels in tumor tissues were determined using immunohistochemical labeling. XHP demonstrated anticancer effects on BC cells by suppressing cell proliferation, inducing cellular apoptosis, and inhibiting EMT progression. XHP may regulate the EMT via the TGF-β axis, as shown by RNA sequencing and Western blotting analysis. Furthermore, the combination of XHP and Dox had a stronger therapeutic effect on BC cell proliferation, apoptosis, and metastasis in both cellular and animal models. We were the first to reveal that XHP abrogated EMT progression via modulating the TGF-β axis. Furthermore, the combination therapy of XHP and Dox presents a promising novel therapeutic candidate for BC patients. [Display omitted] • XHP suppressed malignancy-related activities in breast cancer cells by inhibiting cellular growth and the progression of epithelial-mesenchymal transition. • XHP combined with Doxorubicin enhanced chemotherapy effectiveness in vitro and in vivo. • XHP attenuated breast cancer metastasis by downregulating the TGF-β signaling pathway. [ABSTRACT FROM AUTHOR]

GeAs 2 is an attractive semiconductor. However, the structure, optical properties and electronic properties of GeAs 2 with Ge-vacancy are unclear. Here, we use the first-principles to investigate the effect of Ge-vacancy on the structure, optical and electronic properties of GeAs 2. Two Ge vacancies are considered here. The results show that V –Ge1 -vacancy is more thermodynamically stable than that of V –Ge2 -vacancy because the bond strength of Ge–As bond for V –Ge1 -vacancy is stronger than that of the V –Ge2 -vacancy. GeAs 2 shows the ultraviolet behavior. In particular, those Ge-vacancies decrease the optical absorption coefficient of GeAs 2. The calculated band gap of GeAs 2 is 0.574eV, indicating that GeAs 2 is a semiconducting. GeAs 2 with those Ge vacancies show metallic behavior because Ge-vacancies promote the electronic transfer near the E F. [ABSTRACT FROM AUTHOR]

Chemotherapy remains a critical component of triple-negative breast cancer (TNBC) treatment; however, patients often develop resistance to chemotherapeutic agents. Accumulating evidence indicates that deubiquitylases (DUBs) play pivotal roles in regulating cell proliferation, differentiation, apoptosis, and tumorigenesis. Deubiquitylase OTUD1 is considered a tumor suppressor in various cancers, yet its role in doxorubicin sensitivity in breast cancer patients remains inadequately understood. In this study, we investigated the expression levels and prognostic role of OTUD1 in breast cancer. Our findings demonstrated that OTUD1 was downregulated in TNBC, and lower OTUD1 expression levels were correlated with poor prognosis. We utilized the CCK-8 cell viability assay, flow cytometric analysis, and a TNBC mouse xenograft model to examine the influence of OTUD1 on doxorubicin (DOX) chemotherapy sensitivity in vitro and in vivo. Western blot and immunohistochemistry were employed to explore the correlation between OTUD1 and P16. Our results indicated that upregulation of OTUD1 expression inhibits TNBC cell proliferation and enhances its sensitivity to doxorubicin. Additionally, rescue experiments confirmed that the chemosensitizing effect of OTUD1 overexpression could be reversed by the inhibition of P16. Therefore, our findings reveal that OTUD1 sensitizes TNBC cells to DOX by upregulating P16 expression, suggesting a potential new diagnostic biomarker and therapeutic target for the future treatment of TNBC. [ABSTRACT FROM AUTHOR]