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Long noncoding RNA CMPK2 promotes colorectal cancer progression by activating the FUBP3-c-Myc axis.
Oncogene ( IF 6.9 ) Pub Date : 2020-03-20 , DOI: 10.1038/s41388-020-1266-8 Qingzu Gao 1, 2, 3 , Rui Zhou 1, 3 , Yuan Meng 1, 4 , Rongfei Duan 5 , Ling Wu 1, 3 , Rui Li 1, 3 , Fengliu Deng 1, 3 , Chuang Lin 1 , Liang Zhao 1, 3
Oncogene ( IF 6.9 ) Pub Date : 2020-03-20 , DOI: 10.1038/s41388-020-1266-8 Qingzu Gao 1, 2, 3 , Rui Zhou 1, 3 , Yuan Meng 1, 4 , Rongfei Duan 5 , Ling Wu 1, 3 , Rui Li 1, 3 , Fengliu Deng 1, 3 , Chuang Lin 1 , Liang Zhao 1, 3
Affiliation
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Long noncoding RNAs (lncRNAs) have been shown to play crucial roles in cancer long noncoding RNAs (lncRNAs) have been known to play crucial roles in cancer development and progression by regulating chromatin dynamics and gene expression. However, only a few lncRNAs with annotated functions in the progression of colorectal cancer (CRC) have been identified to date. In the present study, the expression of lncCMPK2 was upregulated in CRC tissues and positively correlated with clinical stages and lymphatic metastasis. The overexpression of lncCMPK2 promoted the proliferation and cell cycle transition of CRC cells. Conversely, the silencing of lncCMPK2 restricted cell proliferation both in vitro and in vivo. lncCMPK2 was localized to the nucleus of CRC cells, bound to far upstream element binding protein 3 (FUBP3), and guided FUBP3 to the far upstream element (FUSE) of the c-Myc gene to activate transcription. lncCMPK2 also stabilized FUBP3. These results provide novel insights into the functional mechanism of lncCMPK2 in CRC progression and highlight its potential as a biomarker of advanced CRC and therapeutic target.
中文翻译：
长的非编码RNA CMPK2通过激活FUBP3-c-Myc轴来促进结直肠癌的进展。
长非编码RNA（lncRNA）已显示在癌症中起关键作用长非编码RNA（lncRNA）已通过调节染色质动力学和基因表达在癌症发展和进程中发挥关键作用。然而，迄今为止，仅鉴定了少数在大肠癌（CRC）进展中具有注释功能的lncRNA。在本研究中，lncCMPK2在CRC组织中的表达上调，与临床分期和淋巴结转移呈正相关。lncCMPK2的过表达促进了CRC细胞的增殖和细胞周期转变。相反地，lncCMPK2的沉默在体外和体内都限制了细胞的增殖。lncCMPK2定位于CRC细胞核，与远上游元件结合蛋白3（FUBP3）结合，并将FUBP3引导至c-Myc基因的远上游元件（FUSE）以激活转录。lncCMPK2也稳定了FUBP3。这些结果提供了对lncCMPK2在CRC进展中的功能机制的新颖见解，并突出了其作为晚期CRC和治疗靶标的生物标志物的潜力。
更新日期：2020-03-20
中文翻译：
长的非编码RNA CMPK2通过激活FUBP3-c-Myc轴来促进结直肠癌的进展。
长非编码RNA（lncRNA）已显示在癌症中起关键作用长非编码RNA（lncRNA）已通过调节染色质动力学和基因表达在癌症发展和进程中发挥关键作用。然而，迄今为止，仅鉴定了少数在大肠癌（CRC）进展中具有注释功能的lncRNA。在本研究中，lncCMPK2在CRC组织中的表达上调，与临床分期和淋巴结转移呈正相关。lncCMPK2的过表达促进了CRC细胞的增殖和细胞周期转变。相反地，lncCMPK2的沉默在体外和体内都限制了细胞的增殖。lncCMPK2定位于CRC细胞核，与远上游元件结合蛋白3（FUBP3）结合，并将FUBP3引导至c-Myc基因的远上游元件（FUSE）以激活转录。lncCMPK2也稳定了FUBP3。这些结果提供了对lncCMPK2在CRC进展中的功能机制的新颖见解，并突出了其作为晚期CRC和治疗靶标的生物标志物的潜力。
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