Ara-c induces cell cycle G1/S arrest by inducing upregulation of the INK4 family gene or directly inhibiting the formation of the cell cycle-dependent complex CDK4/cyclin D1

Sun Fuze; Li Niannian; Tong Xiaoling; Zeng Jie; He Songzhen; Gai Tingting; Bai Yanmin; Liu Lanlan; Lu Kunpeng; Shen Jianghong; Han Minjin; Lu Cheng; Dai Fangyin

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Ara-c induces cell cycle G1/S arrest by inducing upregulation of the INK4 family gene or directly inhibiting the formation of the cell cycle-dependent complex CDK4/cyclin D1

机译：ARA-C通过诱导Ink4家族基因的上调或直接抑制细胞周期依赖性复合CDK4 / Cyclin D1的形成，诱导细胞周期G1 / s逮捕

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Cytosine arabinoside (Ara-c) is a pyrimidine anti-metabolite that is capable of interfering with cellular proliferation by inhibiting DNA synthesis. Each inhibitor of cyclin-dependent kinase 4 (INK4) family member has the ability to bind to cyclin-dependent kinase 4 (CDK4) and inhibit the formation of the cell cycle-dependent CDK4/cyclin D1 complex, subsequently leading to cell cycle arrest in the G1/S phase. In this study, the expression of INK4 family genes in kidney cancer and the impact of these genes on patient prognosis were examined. Additionally, the effects of INK4 family genes and Ara-c on cell proliferation and tumor formation and development were examined. Finally, a potential association between Ara-c-induced cell cycle arrest and INK4-associated gene expression was evaluated. An upregulation of INK4 family genes was found to be positively correlated with the prognosis of patients with kidney cancer. Both the INK4 family genes and Ara-c were shown to induce cell cycle arrest and inhibit tumor formation and development. Moreover, Ara-c-induced cell cycle arrest was found to be associated with an Ara-c-induced upregulation of INK4 family gene expression, which ultimately inhibited the formation of the CDK4/cyclin D1 complex. These findings suggested that an upregulation of INK4 family genes has a positive effect on kidney cancer prognosis and can inhibit the formation and development of tumors. Moreover, Ara-c was shown to promote the upregulation of INK4 family genes, at the same time, Ara-c could directly regulate the cell cycle-dependent genes CDK4 and cyclin D1 (CCND1), independent of the INK4 family genes.

机译：胞嘧啶阿拉伯核苷（ARA-C）是一种嘧啶抗代谢物，其能够通过抑制DNA合成干扰细胞增殖。周细胞周期蛋白依赖性激酶4（Ink4）家族构件的抑制剂具有结合细胞周期蛋白依赖性激酶4（CDK4）并抑制细胞周期依赖性CDK4 / Cyclin D1复合物的形成，随后导致细胞周期停滞G1 / S期。在这项研究中，检查了肾癌中的Ink4家族基因的表达及这些基因对患者预后的影响。另外，研究了Ink4家族基因和ARA-C对细胞增殖和肿瘤形成和发育的影响。最后，评估ARA-C诱导细胞周期停滞和INK4相关基因表达之间的潜在关联。发现Ink4家族基因的上调与肾癌患者的预后呈正相关。显示INK4家族基因和ARA-C都显示出诱导细胞周期停滞和抑制肿瘤形成和发育。此外，发现ARA-C诱导的细胞周期停滞与INK4家族基因表达的ARA-C诱导的抑制有关，这最终抑制了CDK4 / cyclin D1复合物的形成。这些研究结果表明，Ink4家族基因的上调对肾癌预后的积极影响，并且可以抑制肿瘤的形成和发育。此外，ARA-C显示促进INK4家族基因的上调，同时，ARA-C可以直接调节细胞周期依赖性基因CDK4和细胞周期蛋白D1（CCND1），与INK4家族基因无关。

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来源
《Cell cycle》 |2019年第18期|共14页
作者
Sun Fuze; Li Niannian; Tong Xiaoling; Zeng Jie; He Songzhen; Gai Tingting; Bai Yanmin; Liu Lanlan; Lu Kunpeng; Shen Jianghong; Han Minjin; Lu Cheng; Dai Fangyin;
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作者单位

Southwest Univ Coll Biotechnol Minist Agr State Key Lab Silkworm Genome Biol Key Lab Sericu;

Southwest Univ Coll Biotechnol Minist Agr State Key Lab Silkworm Genome Biol Key Lab Sericu;

Southwest Univ Coll Biotechnol Minist Agr State Key Lab Silkworm Genome Biol Key Lab Sericu;

Southwest Univ Coll Biotechnol Minist Agr State Key Lab Silkworm Genome Biol Key Lab Sericu;

Southwest Univ Coll Biotechnol Minist Agr State Key Lab Silkworm Genome Biol Key Lab Sericu;

Southwest Univ Coll Biotechnol Minist Agr State Key Lab Silkworm Genome Biol Key Lab Sericu;

Southwest Univ Coll Biotechnol Minist Agr State Key Lab Silkworm Genome Biol Key Lab Sericu;

Southwest Univ Coll Biotechnol Minist Agr State Key Lab Silkworm Genome Biol Key Lab Sericu;

Southwest Univ Coll Biotechnol Minist Agr State Key Lab Silkworm Genome Biol Key Lab Sericu;

Southwest Univ Coll Biotechnol Minist Agr State Key Lab Silkworm Genome Biol Key Lab Sericu;

Southwest Univ Coll Biotechnol Minist Agr State Key Lab Silkworm Genome Biol Key Lab Sericu;

Southwest Univ Coll Biotechnol Minist Agr State Key Lab Silkworm Genome Biol Key Lab Sericu;

Southwest Univ Coll Biotechnol Minist Agr State Key Lab Silkworm Genome Biol Key Lab Sericu;

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原文格式 PDF
正文语种 eng
中图分类细胞生物学;
关键词
INK4 family; Ara-c; cell proliferation; cell cycle; CDK4; Cyclin D1;

机译：Ink4家族;ARA-C;细胞增殖;细胞周期;CDK4;CYCLIN D1;

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专利

1. Ara-c induces cell cycle G1/S arrest by inducing upregulation of the INK4 family gene or directly inhibiting the formation of the cell cycle-dependent complex CDK4/cyclin D1 [J] . Sun Fuze, Li Niannian, Tong Xiaoling, Cell cycle . 2019,第18期

机译：ARA-C通过诱导Ink4家族基因的上调或直接抑制细胞周期依赖性复合CDK4 / Cyclin D1的形成，诱导细胞周期G1 / s逮捕
2. Wogonin induces G1 phase arrest through inhibiting Cdk4 and cyclin D1 concomitant with an elevation in p21Cip1 in human cervical carcinoma HeLa cells. [J] . Yang L, Zhang HW, Hu Biochemistry and Cell Biology . 2009,第6期

机译：Wogonin通过抑制Cdk4和cyclin D1诱导G1期停滞，并伴随人类宫颈癌HeLa细胞中p21Cip1升高。
3. Blockade of Rac1 activity induces G1 cell cycle arrest or apoptosis in breast cancer cells through downregulation of cyclin D1, survivin, and X-linked inhibitor of apoptosis protein. [J] . Yoshida T, Zhang Y, Rivera Rosado LA, Molecular cancer therapeutics . 2010,第6期

机译：Rac1活性的阻断通过下调细胞周期蛋白D1，survivin和X连锁的凋亡蛋白抑制剂诱导乳腺癌细胞G1周期停滞或凋亡。
4. Adenosine induces G2/M cell-cycle arrest by inhibiting cell mitosis progress [C] . Jia Kun-Zhi, Tang Bo, Yu Lu, International Symposium on Medical and Pharmaceutical Biotechnology(医药生物技术国际研讨会) . 2009

机译：腺苷通过抑制细胞有丝分裂进程诱导G2 / M细胞周期停滞
5. The candidate tumour suppressor, XIAP associated factor 1 (XAF1), directly inhibits XIAP activity and induces G1 phase cell cycle arrest. [D] . Fong, Wai Gin. 2003

机译：候选肿瘤抑制物XIAP相关因子1（XAF1）直接抑制XIAP活性并诱导G1期细胞周期停滞。
6. Subtilase cytotoxin produced by Shiga-toxigenic Escherichia coli transiently inhibits protein synthesis of Vero cells via degradation of BiP and induces cell cycle arrest at G1 by downregulation of cyclin D1 [O] . Naoko Morinaga, Kinnosuke Yahiro, Gen Matsuura, -1

机译：志贺毒素大肠杆菌产生的枯草杆菌细胞毒素通过BiP的降解瞬时抑制Vero细胞的蛋白质合成并通过下调细胞周期蛋白D1诱导在G1处的细胞周期停滞
7. Blockade of Rac1 Activity Induces G1 Cell Cycle Arrest or Apoptosis in Breast Cancer Cells through Downregulation of Cyclin D1, Survivin, and X-Linked Inhibitor of Apoptosis Protein [O] . Tatsushi Yoshida, Yaqin Zhang, Leslie A. Rivera Rosado, 2010

机译：通过下调细胞周期蛋白D1，Survivin和凋亡蛋白的X键抑制剂，封闭Rac1活性在乳腺癌细胞中诱导G1细胞周期停滞或细胞凋亡

Ara-c induces cell cycle G1/S arrest by inducing upregulation of the INK4 family gene or directly inhibiting the formation of the cell cycle-dependent complex CDK4/cyclin D1

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