Breast cancer has become the malignant tumor with the first incidence and the second mortality among female cancers. Most female breast cancers belong to luminal-type breast cancer and HER2-positive breast cancer. These breast cancer cells all have different driving genes, which constantly promote the proliferation and metastasis of breast cancer cells. Signal transducer and activator of transcription 3 (STAT3) is an important breast cancer-related gene, which can promote the progress of breast cancer. It has been proved in clinical and basic research that over-expressed and constitutively activated STAT3 is involved in the progress, proliferation, metastasis and chemotherapy resistance of breast cancer. STAT3 is an important key target in luminal-type breast cancer and HER2-positive cancer, which has an important impact on the curative effect of related treatments. In breast cancer, the activation of STAT3 will change the spatial position of STAT3 protein and cause different phenotypic changes of breast cancer cells. In the current basic research and clinical research, small molecule inhibitors activated by targeting STAT3 can effectively treat breast cancer, and enhance the efficacy level of related treatment methods for luminal-type and HER2-positive breast cancers.
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http://dx.doi.org/10.1186/s12935-024-03541-9 | DOI Listing |
Front Med (Lausanne)
January 2025
Department of General Surgery, The People's Hospital of Fenghua Ningbo, Ningbo, China.
Background: Breast cancer (BC) is the most common cancer in women in the U.S. and a leading cause of cancer-related deaths.
View Article and Find Full Text PDFFront Pharmacol
January 2025
Department of Pharmacy, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Introduction: Triple-negative breast cancer (TNBC) is the most challenging subtype of breast cancer to treat. While previous studies have demonstrated that ginsenoside Rh2 induces apoptosis in TNBC cells, the specific molecular targets and underlying mechanisms remain poorly understood. This study aims to uncover the molecular mechanisms through which ginsenoside Rh2 regulates apoptosis and proliferation in TNBC, offering new insights into its therapeutic potential.
View Article and Find Full Text PDFBreast J
January 2025
Tianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenvironment, Tianjin Lung Cancer Institute, Tianjin Medical University General Hospital, Tianjin 300052, China.
Collagen type XI alpha 1 (COL11A1), a critical member of the collagen superfamily, is essential for tissue structure and integrity. This study aimed to validate previously identified variations in COL11A1 expression during breast cancer carcinogenesis and progression, as well as elucidate their clinical implications. COL11A1 mRNA expression levels were assessed using real-time reverse transcription-PCR (RT-PCR) in 30 pairs of normal breast tissue and primary breast cancer, 30 pairs of primary breast cancer and lymph node metastases, 30 benign tumors, and 107 primary breast cancers.
View Article and Find Full Text PDFOpen Life Sci
December 2024
Department of Pathology, Hangzhou Women's Hospital, 369 Kunpeng Road, Shangcheng District, Hangzhou, 310008, Zhejiang, China.
Breast cancer is a common malignant tumor of women. Ki67 is an important biomarker of cell proliferation. With the quantitative analysis, it is an important indicator of malignancy for breast cancer diagnosis.
View Article and Find Full Text PDFResearch (Wash D C)
January 2025
Department of Sports Medicine, Huashan Hospital Affiliated to Fudan University, Shanghai 200040, China.
Increasing evidence has shown that physical exercise remarkably inhibits oncogenesis and progression of numerous cancers and exercise-responsive microRNAs (miRNAs) exert a marked role in exercise-mediated tumor suppression. In this research, expression and prognostic values of exercise-responsive miRNAs were examined in breast cancer (BRCA) and further pan-cancer types. In addition, multiple independent public and in-house cohorts, in vitro assays involving multiple, macrophages, fibroblasts, and tumor cells, and in vivo models were utilized to uncover the tumor-suppressive roles of miR-29a-3p in cancers.
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