lncRNA DLX6-AS1在恶性肿瘤中的研究进展

期刊菜单

lncRNA DLX6-AS1在恶性肿瘤中的研究进展
Research Progress of lncRNA DLX6-AS1 in Malignant Tumors

DOI: 10.12677/WJCR.2023.132007, PDF, 下载: 279 浏览: 662 科研立项经费支持
作者: 桂宇欣, 孙杰克, 石玉荣^*：蚌埠医学院检验医学院，安徽蚌埠
关键词: 长链非编码RNAs；DLX6-AS1；恶性肿瘤；研究进展；Long-Chain Non-Coding RNAs； DLX6-AS1； Malignant Tumor； Research Progress

摘要: 长链非编码RNAs表达具备时间特异性和空间特异性。DLX6-AS1是lncRNAs家族中的一员，其表达水平在多种恶性肿瘤中发生显著改变，提示DLX6-AS1在肿瘤的发生、发展和预后中发挥作用。文章对近５年国内外关于DLX6-AS1在恶性肿瘤中的研究进行综述，以期为恶性肿瘤的诊断和潜在治疗靶点选择提供参考。

Abstract: The expression of long-chain noncoding RNAs is time-specific and space-specific. DLX6-AS1 is a member of the lncRNAs family, and its expression level has changed significantly in a variety of malignant tumors, suggesting that DLX6-AS1 plays a role in the occurrence, development and prognosis of tumors. This article reviews the research on DLX6-AS1 in malignant tumors at home and abroad in the past five years, in order to provide reference for the diagnosis of malignant tumors and the selection of potential therapeutic targets.

文章引用：桂宇欣, 孙杰克, 石玉荣. lncRNA DLX6-AS1在恶性肿瘤中的研究进展[J]. 世界肿瘤研究, 2023, 13(2): 44-50. https://doi.org/10.12677/WJCR.2023.132007

1. 引言

长链非编码RNAs (long non-coding RNAs, lncRNAs)广泛存在于基因组中，最初被认为是“噪音”，随着对lncRNAs的研究逐步深入，发现其具有多种重要的生物学功能，作为癌基因或抑制基因，在人类疾病的病理生理学中发挥重要作用 [1] 。lncRNA DLX6-AS1是一个新发现的定位于人染色体7q21.3的非编码RNA转录本，长度约为1990 nt。越来越多的研究表明DLX6-AS1在多种肿瘤组织中表达上调，并与肿瘤侵袭和转移有关 [2] [3] [4] [5] 。本文就lncRNA DLX6-AS1在恶性肿瘤中作用机制的相关研究进展文献综述如下，以期为恶性肿瘤的诊断和潜在治疗靶点的选择提供参考。

2. lncRNAs的生物学特征

LncRNAs是一类长度超过200个核苷酸的非编码RNA，在进化上相对保守，且大多数lncRNAs并不具备编码蛋白质的功能 [6] 。lncRNAs可作为转录后调节子、增强子、剪接调节器和染色体修饰物等参与大多数细胞的生理过程。目前的研究已经证明，lncRNAs是一种关键的表观遗传修饰因子，通过与染色质、蛋白质和RNA靶标的相互作用，调控基因的表达。lncRNAs通过招募特异的染色质复合体而发挥表观遗传修饰，也可通过与靶基因直接作用，对基因表达进行正性或负性调控 [7] 。lncRNAs可作为重要的信号分子，发挥向导功能，充当支架或分子诱饵等作用，使信号通路的特异性成为可能，级联介导某些特异性事件的发生，如肿瘤 [8] 。

3. lncRNAs与肿瘤的关系

LncRNAs可作为肿瘤的癌基因或抑癌基因在不同肿瘤中发生作用，有望成为肿瘤的诊断工具或治疗靶点。在宫颈癌中lncRNA MIAT在宫颈癌组织和细胞系中上调，MIAT靶向调控PI3K表达进而调节Akt、mTOR信号通路相关分子表达，影响细胞调增殖、迁移和侵袭 [9] 。干扰乳腺癌细胞LINC00665表达，乳腺癌细胞中EMT相关基因的表达表达下调 [10] 。食管癌组织和外泌体中lncRNA UCA1的表达下调，可作为食管癌潜在的生物标志物用于食管癌的临床诊断 [11] 。lncRNA TUSC8TUSC8作为miR-190b-5p的分子海绵，抑制乳腺癌转移，而成为乳腺癌治疗的潜在靶点 [12] 。

4. lncRNA DLX6-AS1与恶性肿瘤

4.1. lncRNA DLX6-AS1与肺癌

肺癌是最常见的肺原发性恶性肿瘤，主要治疗策略仍以手术切除为主，合并化疗、放疗及靶向治疗等，而无有效的对因治疗方法，因此寻找灵敏度更高的分子标志物是目前待解决的问题之一。

Sun W等人利用RT-PCR检测发现lncRNA DLX6-AS1在NSCLC组织中过表达，且与肿瘤大小和临床分期有关；DLX6-AS1通过下调miR-27b-3p表达，进而上调GSPT1表达，促进NSCLC的增殖、迁移 [2] 。Huang YD等人的研究结果也证实DLX6-AS1在NSCLC组织和细胞中高表达。DLX6-AS1下调miR-144表达，进而调控PRR11的表达，进而促进NSCLC恶性进展 [13] 。在NSCLC血清中发现，肿瘤细胞外泌体DLX6-AS1表达明显增加，且与肿瘤分期、肿瘤远处转移和预后相关，提示血清肿瘤细胞外泌体DLX6-AS1可作为NSCLC诊断及预后判断的分子靶标 [3] 。

Wu C等人认为在NSCLC细胞中研究发现，MiR-16-5p是DLX6-AS1的靶点，DLX6-AS1可抑制NSCLC中MiR-16-5p表达。MiR-16-5p与BMI1存在靶向作用，MiR-16-5p上调可下调A549细胞中BMI1表达，提示NSCLC中DLX6-AS1过表达，可抑制miR-16-5p靶向BMI1的抗肿瘤作用 [14] 。

在肺鳞状细胞癌组织和细胞中，DLX6-AS1高表达，在SK-MES1顺铂耐药细胞株中，DLX6-AS1表达明显上调，miR-181a-5p和miR-382-5p表达下调，二者呈负相关。CELF1是miR-181a-5p和miR-382-5p的下游靶基因，干扰miR-181a-5p和miR-382-5p的表达，可上调CELF1的表达，从而介导顺铂耐药SK-MES1对顺铂的敏感性。H3K4me1可诱导DLX6-AS1的表达，可增强肺鳞癌细胞对顺铂的耐药性。这一系列的研究均表明，DLX6-AS1可通过调节miR-181a-5p/miR-382-5p的表达，下调CELF1的表达，从而导致肺鳞癌细胞对顺铂的继发耐药，提示下调DLX6-AS1的表达，可能逆转肺鳞癌细胞顺铂继发耐药，提高顺铂治疗的敏感性 [15] 。

4.2. lncRNA DLX6-AS1与胃癌

胃癌是起源于胃黏膜上皮细胞的恶性病变，是最常见的消化系统恶性肿瘤之一。研究发现lncRNA DLX6-AS1在胃癌组织中高表达，且与胃癌的临床分期、转移和预后相关。干扰胃癌细胞中DLX6-AS1表达，可抑制胃癌细胞中的N-cadherin和Vimetin等EMT标志物表达，抑制细胞迁移转移 [4] 。下调HGC-27细胞DLX6-AS1表达，可下调FUS表达，进一步下调MAP4K1、MAP4K2、MAP4K3和MAP4K4表达，细胞增殖、迁移能力明显下降 [16] 。miR-4290是DLX6-AS1的下游靶点，而miR-4290能靶向调节PDK1的表达，sh-DLX6-AS1和PDK1过表达联合作用，显著增强细胞有氧糖酵解，抑制线粒体呼吸，同时细胞增殖增加，而凋亡明显下调 [17] 。提示在胃癌治疗中DLX6-AS1可作为新的生物靶点。

4.3. lncRNA DLX6-AS1与肝癌

肝癌是世界最常见的恶性肿瘤之一，早期难诊断且死亡率高。Zhang L等人检测了60例肝癌组织及对应的癌旁组织中DLX6-AS1的表达，结果显示肝癌组织中DLX6-AS1高表达，且与肝癌患者预后不良相关。敲除肝癌细胞中DLX6-AS1基因，能有效抑制细胞的恶性生物学行为，并促进肝癌细胞凋亡，抑制体内肿瘤的生长。临床检测血清中DLX6-AS1含量，可用于肝癌的诊断与治疗效果监测。生物学信息分析，miR-203a和DLX6-AS1之间存在靶向作用，DLX6-AS1可靶向调节，miR-203a表达，MMP-2是miR-203a的下游靶基因，提示DLX6-AS1可通过miR-203a/MMP-2途径促进肝癌的发生发展 [5] 。lncRNA DLX6-AS1在肝癌中的高表达，上调lncRNA DLX6-AS1，肝癌细胞阻滞在G0/G1期。miR-424-5p和DLX6-AS1存在结合位点，且癌基因WEE1 G2检查点激酶(WEE1)是miR-424-5p的靶点，肝癌细胞DLX6-AS1表达上调，抑制miR-424-5p表达，降低miR-424-5p对WEE1的表达抑制作用，进而促进肝癌细胞的恶性表型 [18] 。

Liu X等人研究发现，下调肝癌细胞株中lncRNA DLX6-AS1，能上调miR-513c表达，下调Cul4A的表达，而Cul4A的沉默又可抑制ANXA10降解，进而抑制肝癌细胞的恶性表型，证实DLX6-AS1可通过靶向miR-513c上调Cul4A表达，从而增加肝癌细胞的增殖、迁移能力 [19] 。提示DLX6-AS1可作为癌基因，促进肝癌的恶性进展，也为肝癌的治疗提供新的视野。

4.4. lncRNA DLX6-AS1与胰腺癌

胰腺癌是最具侵袭性的恶性肿瘤之一。DLX6-AS1在胰腺癌中表达上调，且与肿瘤的不良预后相关。MiR-181b是DLX6-AS1的下游靶点，干扰胰腺癌细胞DLX6-AS1表达，能显著上调胰腺癌细胞MiR-181b表达。转染MiR-181b类似物，能显著下调胰腺癌细胞ZEB2表达，siDLX6-AS1和MiR-181b抑制剂联合作用，ZEB2表达明显增加，E-cadherin表达上调，提示MiR-181b抑制剂能有效抑制DLX6-AS1对胰腺癌细胞的EMT作用 [20] 。Yang J等人的研究结果与An Y等人的研究结果相似，DLX6-AS1表达胰腺癌的不良预后相关，且DLX6-AS1的表达上调，促进胰腺癌细胞增殖迁移。过表达DLX6-AS1可下调胰腺癌细胞miR-497-5p表达。转染miR-497-5p类似物，胰腺癌细胞FZD4和FZD6表达明显下调，miR-497-5p能通过调节FZD4和FZD6表达，影响细胞的增殖迁移 [21] ，提示DLX6-AS1提示可能是胰腺癌的潜在生物标志物。

4.5. lncRNA DLX6-AS1与结直肠癌

结直肠癌是最常见的胃肠道肿瘤，是全球癌症相关死亡的主要原因之一。Zhang JJ等人研究发现结直肠癌组织中DLX6-AS1表达上调，且与预后不良相关。DLX6-AS1在HCT116细胞中表达上调，通过PI3K/AKT/mTOR信号通路促进细胞增殖、侵袭和迁移，抑制细胞凋亡 [22] 。干扰DLX6-AS1表达，miR-26a表达增加，miR-26a下游靶基因EZH2表达减少，细胞增殖迁移抑制提示DLX6-AS1可靶向miR-26a进而调节EZH2表达，调节细胞增殖迁移和EMT [23] 。

4.6. lncRNA DLX6-AS1与膀胱癌

膀胱癌是人类最常见的泌尿系统恶性肿瘤，预后较差。膀胱癌组织中DLX6-AS1高表达，下调膀胱癌细胞DLX6-AS1表达，可通过EMT和Wnt/β-catenin信号通路抑制细胞的增殖迁移作用 [24] 。miR-195-5p是DLX6-AS1的靶点，干扰DLX6-AS1表达，miR-195-5p表达上调，VEGFA表达下调，提示DLX6-AS1可靶向调控miR-195-5p/VEGFA表达影响肿瘤细胞的恶性表型 [25] 。在Fang C等人的研究中发现，lncRNA DXL6-AS1在膀胱癌组织可靶向调节miR-223表达，转染miR-223类似物，肿瘤细胞的增殖和侵袭能力明显下调，提示DXL6-AS1对肿瘤细胞的增殖迁移作用，可被miR-223的过表达逆转 [26] 。

4.7. lncRNA DLX6-AS1与妇科恶性肿瘤

宫颈癌是原发于子宫颈组织的恶性肿瘤，严重威胁着女性的健康和生命。有研究表明宫颈癌患者的血清外源性lncRNA DLX6-AS1水平显著升高，并与肿瘤的不良预后呈正相关，提示外泌体lncRNA DLX6-AS1可作为宫颈癌的潜在的诊断和预测预后额分子靶标 [27] 。DLX6-AS1是miR-16-5p的海绵并能下调宫颈癌组织中miR-16-5p表达，上调ARPP19表达，从而调节肿瘤的增殖迁移能力 [28] 。在Wang X等人研究中证实DLX6-AS1能靶向调控miR-199a表达，影响宫颈癌细胞的恶性生物学行为 [29] 。DLX6-AS1在子宫内膜癌组织和细胞中高表达，与p300/E2F1乙酰转移酶相互作用，促进子宫内膜癌的恶性表型 [30] 。在卵巢癌组织和细胞系中DLX6-AS1表达增加，且与不良预后相关。干扰DLX6-AS1表达，卵巢癌细胞Notch信号通路相关分子表达明显下调，细胞增殖、迁移及侵袭水平下调 [31] 。

4.8. lncRNA DLX6-AS1与其他肿瘤

前列腺癌已成为全球男性癌症相关死亡的第二大原因。前列腺癌组织和细胞中DLX6-AS1表达明显增加，且与miR-497-5p表达存在负相关，提示DLX6-AS1可能靶向调控miR-497-5p表达而发挥癌基因的作用。突触核蛋白γ (SNCG)是miR-497-5p的下游靶基因，DLX6-AS1可通过miR-497-5/SNCG信号通路表达调控细胞恶行表型 [32] 。

乳腺癌是一种发生于乳腺组织中的恶性肿瘤。乳腺癌组织中，DLX6-AS1m表达上调，与miR-505-3p表达呈负相关，提示DLX6-AS1可能通过下调miR-505-3p表达影响乳腺癌细胞的恶性生物学行为 [33] 。DLX6-AS1在三阴性乳腺癌组织和细胞系中表达上调，EMT相关蛋白表达亦明显上调。干扰DLX6-AS1表达，miR-199b-5p表达明显上调，PXN表达下调。三阴性乳腺癌DLX6-AS1表达上调，顺铂IC50增加，提示DLX6-AS1与三阴性乳腺癌顺铂治疗耐药相关 [34] 。

喉癌是头颈部癌症中最常见的肿瘤类型。Liu Y等人研究发现喉癌组织中lncRNA DLX6-AS1高表达，且与肿瘤的临床分期有关，lncRNA DLX6-AS1高表达患者预后不良。干扰DLX6-AS1基因表达，细胞增殖能力下调，细胞凋亡增加。DLX6-AS1可调节HEp-2细胞miR-26a表达，并进一步调控TRPC3表达，影响HEp-2细胞线粒体对钙的摄取，影响细胞增殖与凋亡 [35] 。MiR-376c与DLX6-AS1下调喉鳞状细胞癌细胞中MiR-376c表达，敲除DLX6-AS1，可使Hep2细胞中miR-376c的表达增强，抑制细胞增殖、并使细胞阻滞在G1期 [36] 。

5. 总结与展望

lncRNA DLX6-AS1在肺癌、胃癌、肝癌、胰腺癌等恶性肿瘤中表达上调，可作为癌基因参与多种恶性肿瘤的发生、发展，且与肿瘤患者的临床分期和预后相关，可作为新型的肿瘤标志物可用于肿瘤的早期诊断、肿瘤分期分级与预后判断等，具有较高的临床应用价值。然而，DLX6-AS1在不同恶性肿瘤中的作用机制尚未完全明确，因此进一步研究其作用机制，对DLX6-AS1成为恶性肿瘤诊断及治疗的新靶点具有重要意义。

基金项目

安徽省教育厅自然科学研究重点项目(KJ2021A0713)；

安徽省大学生创新教育训练计划项目(S202110367068)。

NOTES

^*通讯作者。

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