• Mashup Score: 8

    Endocrine resistance is a major challenge in the treatment of estrogen receptor-positive (ER+) breast cancer, often leading to disease recurrence and metastasis. 3β-Hydroxysteroid dehydrogenase 1 (3βHSD1, encoded by HSD3B1) catalyzes the rate-limiting conversion of dehydroepiandrosterone (DHEA) to androstenedione (AD), the major substrate for aromatase and a key precursor for estrogen biosynthesis. However, the regulation of HSD3B1 in endocrine-resistant breast cancer remains unclear. We show that long-term estrogen deprivation (LTED) or tamoxifen treatment induces HSD3B1 expression and enzymatic activity, sustaining DHEA metabolism and ER signaling in resistant ER+ breast cancer cells.

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    • Congrats @li_xiuxiu_ on her story just out @jbiolchem @ASBMB! HSD3B1 Upregulation via LRH1 Sustains Estrogen Receptor Signaling and Promotes Endocrine Resistance in Breast Cancer - Journal of Biological Chemistry @dsui_miami_uro @SylvesterCancer https://t.co/bKXuHKQNV2

  • Mashup Score: 1

    Periodontitis is a prevalent chronic inflammatory disease characterized by alveolar bone resorption mediated by osteoclasts. Pyruvate kinase M2 (PKM2), a key enzyme in glycolysis and pyruvate metabolism, has recently been recognized for its regulatory roles beyond metabolism, including gene expression and protein kinase activity. However, its exact role in osteoclastogenesis remains unclear. This study investigates the function of PKM2 in inflammatory osteoclastogenesis and explores its potential as a therapeutic target for periodontitis.

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    • Li et al.'s findings reveal that PKM2 regulates inflammatory osteoclastogenesis through modulation of glycolysis and STAT3 signaling. https://t.co/64PLCKEflB

  • Mashup Score: 0

    The chemokine receptor CCR9 coordinates immune cell migration from the thymus to the small intestine along gradients of the chemokine CCL25. Receptor dysregulation is associated with a variety of inflammatory bowel diseases such as Crohn’s and ulcerative colitis, while aberrant CCR9 overexpression correlates with tumor metastasis. Despite being an attractive therapeutic target, attempts to clinically antagonize CCR9 have been unsuccessful. This highlights the need for a deeper understanding of its specific regulatory mechanisms and signaling pathways.

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    • Lamme et al. identified specific phosphorylation motifs that attenuate G protein coupling. https://t.co/1DWrU8pl2R