Publications by authors named "Tise Suzuki"
To understand chemoresistance in the context of cancer stem cells (CSC), a cisplatin resistance model was developed using a high-grade serous ovarian cancer patient-derived, cisplatin-sensitive sample, PDX4. As a molecular subtype-specific stem-like cell line, PDX4 was selected for its representative features, including its histopathological and mutation status, and exposed to cisplatin in vitro. In the cisplatin-resistant cells, transcriptomics were carried out, and cell morphology, protein expression, and functional status were characterized.
View Article and Find Full Text PDFOvarian cancer remains the most lethal gynecologic malignancy in the USA. For over twenty years, epithelial-mesenchymal transition (EMT) has been characterized extensively in development and disease. The dysregulation of this process in cancer has been identified as a mechanism by which epithelial tumors become more aggressive, allowing them to survive and invade distant tissues.
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- Patients with advanced prostate cancer often develop resistance to common treatments like anti-androgen therapy and chemotherapy.
- The glucocorticoid receptor (GR) and the co-activator LEDGF/p75 are linked to this resistance, as changes in GR levels affect LEDGF/p75 expression in prostate cancer cells.
- Targeting the GR-LEDGF/p75 pathway could enhance chemotherapy sensitivity, suggesting new therapeutic approaches for treating advanced prostate cancer.
The marine pathogen Vibrio vulnificus senses and responds to environmental stimuli via two chemosensory systems and 42-53 chemoreceptors. Here, we present an analysis of the V. vulnificus Aer2 chemoreceptor, VvAer2, which is the first V.
View Article and Find Full Text PDFHigh-grade serous carcinoma of the ovary is a deadly gynecological cancer with poor long-term survival. Dysregulation of microRNAs has been shown to contribute to the formation of cancer stem cells (CSCs), an important part of oncogenesis and tumor progression. The family of microRNAs has previously been shown to regulate stemness and has tumor suppressive actions in a variety of cancers, including ovarian.
View Article and Find Full Text PDFWe aimed to determine the mechanism of epithelial-mesenchymal transition (EMT)-induced stemness in cancer cells. Cancer relapse and metastasis are caused by rare stem-like cells within tumors. Studies of stem cell reprogramming have linked repression and acquisition of stemness with the EMT factor, .
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- Patient-derived samples offer a more reliable model for studying high-grade serous ovarian cancer (HGSOC) compared to traditional cell line models, as they accurately reflect the in vivo characteristics of the disease.
- Researchers characterized patient-derived xenograft (PDX) models, discovering that samples exhibited a hybrid of epithelial and mesenchymal traits, impacting their self-renewal and tumorigenicity.
- A notable finding was the inverse relationship between let-7 microRNA and stemness, suggesting that lower let-7 levels correlate with greater tumorigenic potential and sensitivity to chemotherapy, while also indicating that stemness and invasiveness can be dissociated in HGSOC cells.