Publications by authors named "Kouki Tsuboi"

Article Synopsis
  • Triple-negative breast cancer (TNBC) shows aggressive behavior and poor prognosis, prompting research into new treatments; this study investigates resveratrol (RSV) as a potential therapeutic agent.* -
  • RSV treatment led to changes in TNBC cell morphology, reduced migration, and increased signs of cellular aging; it also enhanced the effects of the drug ABT263, which targets specific proteins to induce cell death.* -
  • The findings suggest RSV might be valuable for managing TNBC by lowering metastatic potential and boosting the effectiveness of ABT263 through the up-regulation of key proteins, CDH1 and CDKN1A, via epigenetic changes.*
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Background: Cyclin-dependent kinase (CDK) 4/6 inhibitors represent a significant advancement in the treatment of estrogen receptor (ER)-positive human epidermal growth factor receptor 2-negative advanced breast cancer. However, mechanisms of alterations after acquired resistance to CDK4/6 inhibitors and the optimal treatment options are still not established.

Methods: Abemaciclib-resistant cell lines were established from the models of estrogen deprivation-resistant cell lines which retained ER expression and activated ER function derived from MCF-7 breast cancer cell lines.

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Background: Hormonal therapy is an effective treatment for luminal-like breast cancer. Aromatase inhibitor (AI) is widely used for estrogen receptor-positive, postmenopausal breast cancers. However, resistance is occurred and becomes a serious clinical concern.

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In addition to genomic signaling, Estrogen receptor alpha (ERα) is associated with cell proliferation and survival through extranuclear signaling contributing to endocrine therapy (ET) resistance. However, the relationship between extranuclear ERα and ET resistance has not been extensively studied. We sought to measure extranuclear ERα expression by immunohistochemistry using phosphor-integrated dots (IHC-PIDs) and to assess its predictive value for ET resistance.

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Background: Presently, hormonal therapy targeting estrogen receptors is the most effective treatment available for luminal breast cancer. However, many patients relapse after the therapy. It has been suggested that cancer stem-like cells are involved with hormonal therapy resistance; in the present study, we evaluated this hypothesis.

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Article Synopsis
  • Hormone therapy targeting estrogen receptors is the main treatment for ER-positive breast cancer, but some patients develop resistance, making it a significant challenge.
  • The study explored the relationship between the estrogen receptor and the insulin-like growth factor (IGF) pathway, finding that inhibiting IGF1R can impact growth in hormone-resistant breast cancer cells.
  • Results indicate that blocking the IGF pathway could be a promising new approach for treating ER-positive breast cancer, even when traditional hormone therapies aren't effective.
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We previously reported the establishment of several types of long-term estrogen-depleted-resistant (EDR) cell lines from MCF-7 breast cancer cells. Type 1 EDR cells exhibited the best-studied mechanism of aromatase inhibitor (AI) resistance, in which estrogen receptor (ER) expression remained positive and PI3K signaling was upregulated. Type 2 EDR cells showed reduced ER activity and upregulated JNK-related signaling.

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Hormone therapy is the most effective treatment for patients with estrogen receptor α-positive breast cancers. However, although resistance occurs during treatment in some cases and often reflects changed estrogen receptor α status, the relationship between changes in estrogen receptor α expression and resistance to therapy are poorly understood. In this study, we identified a mechanism for altered estrogen receptor α expression during disease progression and acquired hormone therapy resistance in aromatase inhibitor-resistant breast cancer cell lines.

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Approximately 70% of breast cancers express estrogen receptor α (ERα), which plays critical roles in breast cancer development. Fulvestrant has been effectively used to treat ERα-positive breast cancer, although resistance remains a critical problem. To elucidate the mechanism of resistance to fulvestrant, we established fulvestrant-resistant cell-lines named MFR (MCF-7 derived fulvestrant resistance) and TFR (T-47D derived fulvestrant resistance) from the ERα-positive luminal breast cancer cell lines MCF-7 and T-47D, respectively.

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