Abstract：
BACKGROUND: Ovarian cancer is a malignant tumor of the female reproductive system, and its mortality rate is as high as 70%. Estrogen receptor α (ERα)-positive ovarian cancer accounted for most of all ovarian cancer patients. ERα can promote the growth and proliferation of tumors.
METHODS: The combined effect of All-trans retinoic acid (ATRA) and tamoxifen was obtained by the combination screening of tamoxifen and compound library by MTS. In addition, colony formation assay, flow cytometry analysis, immunofluorescence staining, quantitative real-time polymerase chain reaction (PCR), western blot, and tumor xenotransplantation models were used to further evaluate the efficacy of tamoxifen and ATRA in vitro and in vivo for ER-α-positive ovarian cancer.
RESULTS: In our study, we found that All-trans retinoic acid (ATRA) can cooperate with tamoxifen to cause cell cycle arrest and apoptosis and inhibit ERα-positive ovarian cancer in vivo and in vitro. Further exploration of the mechanism found that ATRA can Inhibit genes related to the ERα signaling pathway, enhance the sensitivity of ERα-positive ovarian cancer cells to tamoxifen, and ascertain the effectiveness of tamoxifen and ATRA as treatments for ovarian cancer with an ERα-positive status.
CONCLUSIONS: Combination of ATRA and tamoxifen is a new way for the treatment of ERα-positive ovarian cancer.
METHODS: The combined effect of All-trans retinoic acid (ATRA) and tamoxifen was obtained by the combination screening of tamoxifen and compound library by MTS. In addition, colony formation assay, flow cytometry analysis, immunofluorescence staining, quantitative real-time polymerase chain reaction (PCR), western blot, and tumor xenotransplantation models were used to further evaluate the efficacy of tamoxifen and ATRA in vitro and in vivo for ER-α-positive ovarian cancer.
RESULTS: In our study, we found that All-trans retinoic acid (ATRA) can cooperate with tamoxifen to cause cell cycle arrest and apoptosis and inhibit ERα-positive ovarian cancer in vivo and in vitro. Further exploration of the mechanism found that ATRA can Inhibit genes related to the ERα signaling pathway, enhance the sensitivity of ERα-positive ovarian cancer cells to tamoxifen, and ascertain the effectiveness of tamoxifen and ATRA as treatments for ovarian cancer with an ERα-positive status.
CONCLUSIONS: Combination of ATRA and tamoxifen is a new way for the treatment of ERα-positive ovarian cancer.
摘要：
背景：卵巢癌是女性生殖系统的恶性肿瘤，其死亡率高达70%。雌激素受体α（ERα）阳性的卵巢癌占所有卵巢癌患者的大多数。ERα可以促进肿瘤的生长和增殖。
方法：通过MTS联合筛选他莫昔芬和化合物库，获得全反式维甲酸（ATRA）和他莫昔芬的联合作用。此外,集落形成试验,流式细胞术分析,免疫荧光染色，定量实时聚合酶链反应（PCR），westernblot,和肿瘤异种移植模型用于进一步评估他莫昔芬和ATRA在体外和体内对ER-α阳性卵巢癌的疗效。
结果：在我们的研究中，我们发现全反式维甲酸（ATRA）在体内和体外可以与他莫昔芬协同作用，引起细胞周期停滞和凋亡，并抑制ERα阳性的卵巢癌。进一步探索机制发现ATRA能够抑制ERα信号通路相关基因,增强ERα阳性卵巢癌细胞对他莫昔芬的敏感性，并确定他莫昔芬和ATRA作为ERα阳性状态的卵巢癌治疗的有效性。
结论：ATRA联合他莫昔芬是治疗ERα阳性卵巢癌的新方法。
方法：通过MTS联合筛选他莫昔芬和化合物库，获得全反式维甲酸（ATRA）和他莫昔芬的联合作用。此外,集落形成试验,流式细胞术分析,免疫荧光染色，定量实时聚合酶链反应（PCR），westernblot,和肿瘤异种移植模型用于进一步评估他莫昔芬和ATRA在体外和体内对ER-α阳性卵巢癌的疗效。
结果：在我们的研究中，我们发现全反式维甲酸（ATRA）在体内和体外可以与他莫昔芬协同作用，引起细胞周期停滞和凋亡，并抑制ERα阳性的卵巢癌。进一步探索机制发现ATRA能够抑制ERα信号通路相关基因,增强ERα阳性卵巢癌细胞对他莫昔芬的敏感性，并确定他莫昔芬和ATRA作为ERα阳性状态的卵巢癌治疗的有效性。
结论：ATRA联合他莫昔芬是治疗ERα阳性卵巢癌的新方法。
