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Mammary Cell News
IGF2BP2 Drives Cell Cycle Progression in Triple-Negative Breast Cancer by Recruiting EIF4A1 to Promote the m6A-Modified CDK6 Translation Initiation Process
[Advanced Science] Investigators found that IGF2BP2 was highly expressed in TNBC due to the lower methylation level in its promoter region.
Mammary Cell News
Identification of a Targetable JAK-STAT Enriched Androgen Receptor and Androgen Receptor Splice Variant Positive Triple-Negative Breast Cancer Subtype
[Cell Reports] Scientists showed that a cohort of TNBC not only expressed androgen receptor (AR) at a much higher rate (∼80%) but also expressesd AR splice variants (∼20%), further subclassifying luminal AR-TNBC.
Mammary Cell News
LncRNA SEMA3B-AS1 Suppresses the Tumor-Initiating Characteristics of Triple Negative Breast Cancer via Engaging in MLL4-Mediated H3K4 Trimethylation
[Molecular Carcinogenesis] Researchers found that low expression of lncRNA SEMA3B-AS1 correlated with unfavorable survival in breast cancer patients. SEMA3B-AS1 was also downregulated in TNBC and linked to advanced tumor stage.
Cancer Stem Cell News
BMI1 Silencing Liposomes Suppress Postradiotherapy Cancer Stemness against Radioresistant Hepatocellular Carcinoma
[ACS Nano] Researchers clarified the relationship between radiotherapy and cancer stemness and provided insights to achieve complete suppression of radioresistant hepatocellular carcinoma tumor by inhibiting cancer stemness.
Mammary Cell News
TNFRSF19 Promotes Endoplasmic Reticulum Stress-Induced Paraptosis via the Activation of the MAPK Pathway in Triple-Negative Breast Cancer Cells
[Cancer Gene Therapy] Scientists demonstrated that the upregulation of TNFRSF19 functioned as a tumor suppressor in TNBC by stimulating paraptosis through the activation of the MAPK pathway-mediated endoplasmic reticulum stress.
Extracellular Matrix News
Chemokines Form Complex Signals During Inflammation and Disease That Can Be Decoded by Extracellular Matrix Proteoglycans
[Science Signaling] Investigators showed that these chemokines differentially interacted with ECM glycosaminoglycans (GAGs), which was enhanced by sulfation of specific GAGs.