Glycogen synthase kinase-3 inhibitors suppress the AR-V7-mediated transcription and selectively inhibit cell growth in AR-V7-positive prostate cancer cells

Nakata Daisuke; Koyama Ryokichi; Nakayama Kazuhide; Kitazawa Satoshi; Watanabe Tatsuya; Hara Takahito

首页> 外文期刊>The Prostate >Glycogen synthase kinase-3 inhibitors suppress the AR-V7-mediated transcription and selectively inhibit cell growth in AR-V7-positive prostate cancer cells

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Glycogen synthase kinase-3 inhibitors suppress the AR-V7-mediated transcription and selectively inhibit cell growth in AR-V7-positive prostate cancer cells

机译：糖原合成酶激酶-3抑制剂抑制Ar-V7介导的转录，并选择性地抑制Ar-V7阳性前列腺癌细胞中的细胞生长

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BACKGROUNDRecent evidence suggests that androgen receptor (AR) splice variants, including AR-V7, play a pivotal role in resistance to androgen blockade in prostate cancer treatment. The development of new therapeutic agents that can suppress the transcriptional activities of AR splice variants has been anticipated as the next generation treatment of castration-resistant prostate cancer.

机译：背景技术证据表明，雄激素受体（AR）接头变体，包括Ar-V7，在前列腺癌治疗中发挥抗雄激素阻滞的抗病作用。可以抑制Ar抗裂解变体的转录活性的新治疗剂的发展已经预期作为抗阉割前列腺癌的下一代治疗。

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来源
《The Prostate》 |2017年第9期|共7页
作者
Nakata Daisuke; Koyama Ryokichi; Nakayama Kazuhide; Kitazawa Satoshi; Watanabe Tatsuya; Hara Takahito;
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作者单位

Takeda Pharmaceut Co Ltd Oncol Drug Discovery Unit Muraoka Higashi 2 Chome Fujisawa Kanagawa;

Takeda Pharmaceut Co Ltd Biomol Res Labs Fujisawa Kanagawa Japan;

Takeda Pharmaceut Co Ltd Oncol Drug Discovery Unit Muraoka Higashi 2 Chome Fujisawa Kanagawa;

Takeda Pharmaceut Co Ltd Oncol Drug Discovery Unit Muraoka Higashi 2 Chome Fujisawa Kanagawa;

Takeda Pharmaceut Co Ltd Oncol Drug Discovery Unit Muraoka Higashi 2 Chome Fujisawa Kanagawa;

Takeda Pharmaceut Co Ltd Oncol Drug Discovery Unit Muraoka Higashi 2 Chome Fujisawa Kanagawa;

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原文格式 PDF
正文语种 eng
中图分类生物化学;
关键词
beta-catenin; AR-V7; castration-resistant prostate cancer; glycogen synthase kinase-3;

机译：Beta-catenin;ar-V7;抗阉割前列腺癌;糖原合酶激酶-3;

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专利

1. Glycogen synthase kinase-3 inhibitors suppress the AR-V7-mediated transcription and selectively inhibit cell growth in AR-V7-positive prostate cancer cells [J] . Nakata Daisuke, Koyama Ryokichi, Nakayama Kazuhide, The Prostate . 2017,第9期

机译：糖原合成酶激酶-3抑制剂抑制Ar-V7介导的转录，并选择性地抑制Ar-V7阳性前列腺癌细胞中的细胞生长
2. Selective growth inhibition by glycogen synthase kinase-3 inhibitors in tumorigenic HeLa hybrid cells is mediated through NF-κB-dependent GLUT3 expression [J] . M Watanabe, N Abe, Y Oshikiri, Oncogenesis. . 2012,第7期

机译：糖原合酶激酶3抑制剂在致癌HeLa杂种细胞中的选择性生长抑制是通过NF-κB依赖性GLUT3表达介导的
3. Maintaining glycogen synthase kinase-3 activity is critical for mTOR kinase inhibitors to inhibit cancer cell growth [J] . KooJ., YueP., GalA.A., Cancer research: The official organ of the American Association for Cancer Research, Inc . 2014,第9期

机译：维持糖原合酶激酶3活性对于mTOR激酶抑制剂抑制癌细胞生长至关重要
4. Silencing of the Fatty Acid Synthase Gene by RNA Interference Inhibits Growth and Induces Apoptosis of LNCaP Prostate Cancer Cells [C] . Ellen De Schrijver, Koen Brusselmans, Walter Heyns, International Symposium on Hormonal Carcinogenesis . 2005

机译：通过RNA干扰沉默脂肪酸合成酶基因抑制生长并诱导LNCAP前列腺癌细胞的凋亡
5. Copper Tolfenamic Acid as a Novel Survivin Inhibitor for Suppressing Pancreatic Cancer Cell Growth via Downregulating Sp1 and Sp3 Transcription Factors [D] . Hurtado, Myrna. 2018

机译：铜脱酚酸作为一种新的Survivin抑制剂，用于通过下调SP1和SP3转录因子来抑制胰腺癌细胞生长
6. Selective growth inhibition by glycogen synthase kinase-3 inhibitors in tumorigenic HeLa hybrid cells is mediated through NF-κB-dependent GLUT3 expression [O] . M Watanabe, N Abe, Y Oshikiri, 2012

机译：糖原合酶激酶-3抑制剂在致癌HeLa杂种细胞中的选择性生长抑制是通过NF-κB依赖性GLUT3表达介导的
7. Maintaining Glycogen Synthase Kinase-3 Activity Is Critical for mTOR Kinase Inhibitors to Inhibit Cancer Cell Growth [O] . Junghui Koo, Ping Yue, Anthony A. Gal, 2014

机译：保持糖原合酶激酶-3活性对于MTOR激酶抑制剂至关重要，以抑制癌细胞生长

Glycogen synthase kinase-3 inhibitors suppress the AR-V7-mediated transcription and selectively inhibit cell growth in AR-V7-positive prostate cancer cells

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