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Advances in Clinical Medicine
Vol. 13  No. 09 ( 2023 ), Article ID: 72844 , 6 pages
10.12677/ACM.2023.1392109

三阴性乳腺癌预后标志物的研究进展

孙启航，贾存东*

新疆医科大学附属肿瘤医院日间病房二病区，新疆 乌鲁木齐

收稿日期：2023年8月21日；录用日期：2023年9月15日；发布日期：2023年9月21日

摘要

三阴性乳腺癌(TNBC)作为一种高度异质性肿瘤，因其临床分期晚、复发转移率高、高度侵袭性等为主要特征，在治疗方案的选择上略显单一。而随着对三阴性乳腺癌组学领域的研究，对于治疗上的选择也有了更多的可能性，为了更好地评估治疗效果，我们需要精确的预后生物标志物。本文将从基因多态性、转录因子、蛋白及代谢物质等不同维度来对TNBC预后生物标志物进行综述。

关键词

三阴性乳腺癌，预后，生物标志物

Progress in Prognostic Markers for Triple-Negative Breast Cancer

Qihang Sun, Cundong Jia*

Second Department of Day Ward, Affiliated Cancer Hospital, Xinjiang Medical University, Urumqi Xinjiang

Received: Aug. 21st, 2023; accepted: Sep. 15th, 2023; published: Sep. 21st, 2023

ABSTRACT

As a highly heterogeneous tumor, triple-negative breast cancer (TNBC) has a slightly homogeneous choice of treatment options due to its main characteristics such as late clinical stage, high recurrence and metastasis rate, and highly invasive nature. And with the research in the field of triple-negative breast cancer histology, there are more possibilities for therapeutic choices, and in order to better evaluate the therapeutic effects, we need accurate prognostic biomarkers. In this paper, we will review TNBC prognostic biomarkers from different dimensions, such as gene polymorphisms, transcription factors, proteins and metabolites.

Keywords:Triple-Negative Breast Cancer (TNBC), Prognosis, Biomarker

Copyright © 2023 by author(s) and Hans Publishers Inc.

This work is licensed under the Creative Commons Attribution International License (CC BY 4.0).

http://creativecommons.org/licenses/by/4.0/

1. 引言

三阴性乳腺癌(TNBC)包括一组具有不同组织学、基因组学和免疫学特征的完全不同的疾病，由于缺乏雌激素受体、孕激素受体和人表皮生长因子受体2表达 [1] ，所以在治疗方案的选择上较为受限，目前仍以化疗为主。相较于其他亚型，TNBC具有发病年轻化，高度侵袭性，复发转移率高等特点。尽管TNBC的临床行为更具侵略性，但一些研究现在已经表明，这些癌症患者在新辅助化疗后更频繁地发展为病理完全反应 [1] ，因此为了更好地评估患者的治疗反应，有效的预后标志物成为了我们判断TNBC患者临床转归的重要指标 [2] ，以便更好地为TNBC治疗及改善预后提供参考。

2. 基于基因多态性的预后标志物

2.1. 程序性细胞死亡1基因(PDCD1)的基因多态性

程序性死亡-1 (PD-1)是一种有效的免疫调节分子，负责T细胞活化和外周耐受的负调节 [2] 。既往研究发现PDCD1的多态性与乳腺癌的预后有关联 [3] 。Thomas等人确定了PDCD1的rs11568821 C/T和rs2227981 G/A多态性与三阴性乳腺癌患者(TNBC)临床病理特征之间的关系。rs11568821中CC/CT和rs2227981中GG/AG的存在与TNBC进展风险无关。rs11568821次要等位基因分布与TNBC风险之间的相关性具有临界显著性(P = 0.0619)。rs2227981多态性与G级显著相关(G3, P = 0.0229)。rs2227981的次要等位基因呈现显著性趋势(P = 0.063448)，Ki67 > 20%。其他临床特征(例如年龄)与rs11568821或rs2227981多态性没有显着相关性。结果表明rs2227981与分级有关；因此，PDCD1可用作TNBC的预后标志物 [4] 。

2.2. 端粒酶逆转录酶(TERT)的基因多态性

TERT在维持端粒DNA长度方面起关键作用。rs10069690单核苷酸变体位于TERT的内含子4中，被发现与端粒长度和雌激素受体阴性但非阳性乳腺癌的风险有关 [5] 。Zins等人发现具有TERT rs10069690 TT基因型的三阴性乳腺癌(TNBC)患者的发病年龄明显小于CC基因型的患者。另一方面，rs10069690 CC基因型往往与预后不良有关，并且与ER阳性患者的不良总生存期(OS)显著相关。此外他们还观察到CC基因型与三阴性患者的脑无转移生存率差之间存在非常显著的关联。高TERT表达往往与无病生存率低有关，特别是在三阴性乳腺癌患者中 [5] 。

2.3. 多聚腺苷二磷酸核糖聚合酶-1 (PARP-1)的基因多态性

PARP-1是PARP超家族中研究最广泛的核酶，用作DNA损伤传感器 [6] 。据报道，PARP1表达与乳腺癌患者的临床病理变量和结果相关 [7] 。侵袭性原发性乳腺肿瘤中PARP1的核表达与化疗敏感性相关 [8] 。Fan [9] 研究了272名接受蒽环类/紫杉类辅助化疗的I~III期原发性TNBC患者的PARP1基因多态性与临床病理特征或生存之间的关联。根据年龄、分级、肿瘤大小、淋巴结状况和血管侵犯进行调整后，rs7531668 TA基因型患者的无进展生存期(DFS)明显高于TT基因型患者，5年DFS分别达到了79.3%和69.2% (P = 0.046)。在淋巴结阴性的人群中，rs6664761 CC基因型患者的DFS明显高于TT基因型患者(P = 0.016)。rs7531668 AA基因型患者的DFS低于TT基因型患者(P = 0.015)。在年龄 ≤ 50岁的人群中，rs6664761 TC基因型预测的DFS高于TT基因型(P = 0.042)。因此PARP1基因的多态性可能预测接受蒽环类/紫杉烷类辅助化疗的TNBC患者的DFS。rs6664761 TC基因型预测的DFS优于TT基因型(P = 0.042)。

3. 基于转录因子的预后标志物

3.1. 微小RNA (miRNA)

miRNA做为非编码RNA家族中的一员，在癌症生物学的几乎所有方面都起作用 [10] 。近年来的研究表明，某些miRNA可直接或间接影响TNBC的发生、进展和复发 [11] 。Kristine [12] 等人在复发性和非复发性TNBC组之间得出了9个显著失调的miRNA (P < 0.05)的列表，其中两种miRNA (miR-32和miR-101)在非复发组中高表达，7种miRNA (miR-18b, miR-20a, miR-30d, miR-103, miR-107, miR-223和miR-652)在复发组中高表达。在一项荟萃分析中探讨了六种miR在TNBC中的预后价值，miR-155低表达与低OS相关。miR21高表达可预测低OS，且miR-27a/b、miR-210和miR-454的高表达与较低的OS相关，此外miR-454和miR-374a/b表达水平与DFS相关 [13] 。Fang等人 [14] 表明抑制miR-21的表达可以降低TNBC细胞系的增殖、活力和侵袭力，并促进细胞凋亡。提示miR-21可能成为TNBC诊断和预后的一种新的生物标志物。Chen等人 [15] 通过多项实验发现了miR-199a-5p在TNBC中的肿瘤抑制作用。MiR-199a-5p的过表达通过改变EMT相关基因的表达，如CDH1和DZEB1，抑制了细胞的增殖、转移能力 [15] 。

3.2. 长链非编码RNA (lncRNA)

lncRNA做为非编码RNA家族的另一位明星分子，lncRNA的异常已被证实表现出肿瘤抑制或致癌作用，并在肿瘤的发展中起重要作用 [16] [17] 。lncRNA的表达失调已在包括TNBC在内的许多类型的肿瘤中观察到 [18] 。在一项分析中利用TCGA数据库发现lncRNA MIR100HG在TNBC中高表达 [19] 。TNBC患者中LncRNA MIR100HG的高表达与预后不良有关。MIR100HG基因表达下调可显著抑制TNBC细胞增殖，抑制肿瘤生长 [20] 。此外Luo [21] 等人发现lncRNA LINC01638过表达可显着促进体外乳腺细胞增殖，并与TNBC患者的不良预后相关。Niu等人 [22] 发现，lncRNA NRON通过下调lncRNA Snar (小核因子90 (NF90)相关RNA)抑制癌细胞增殖。

4. 基于蛋白的预后标志物

4.1. SUMO (一种可逆的翻译后修饰)特异性蛋白酶(SENP)

SENP是半胱氨酸蛋白酶，利用其水解酶活性在C末端切割SUMO的前体或非活性形式，以暴露两个甘氨酸残基 [23] 。在多种肿瘤类型中，SENP已被确定为进展和预后的相关生物标志物。Gao [24] 等人发现SENP1在TNBC肿瘤组织中表达较高，且与TNBC预后相关。SENP1的高表达与组织学分级和肿瘤淋巴结浸润有显著相关性。在TNBC肿瘤中，SENP1的表达水平与CSN5、GATA1和ZEB1的表达水平显著相关。SENP1通过CSN5调控ZEB1去泛素化和表达，促进TNBC细胞迁移和侵袭。此外Zhu [25] 等人发现高水平的SENP3是TNBC患者的独立不良预后因素。他们通过细胞功能实验表明，敲低SENP3会导致体外TNBC细胞的生长、侵袭和迁移受到抑制 [25] 。

4.2. Toll样受体3 (TLR3)

TLR3是Toll样受体(TLR)的关键成员 [26] ，不仅在先天免疫和炎症中起着至关重要的作用，而且在抗癌免疫中也起着至关重要的作用 [27] 。其缺失可导致自身免疫性疾病，癌症以及其他病理状况 [28] 。邵志敏等人 [29] 基于FUSCC数据集，发现TLR3在免疫调节(IM)和间充质样(MES)亚型中高表达，而在腔面雄激素受体(LAR)和基底样免疫抑制(BLIS)亚型中低表达。TLR3在TNBC中的高表达预示着FUSCC TNBC队列中有更好的预后。根据组织微阵列的免疫组化显示，TLR3在乳腺癌组织中的表达低于正常组织。此外，TLR3表达与B细胞、CD4+T细胞、CD8+T细胞、中性粒细胞、巨噬细胞和骨髓树突状细胞呈正相关。

4.3. 分泌性酸性蛋白(SPARC)

SPARC (也称为骨连蛋白或基底膜40, BM40)是一种钙离子结合糖蛋白 [30] 。在肿瘤中，SPARC的主要来源于邻近基质细胞的分泌，而肿瘤细胞分泌较少。Mallavialle [31] 等人发现组织蛋白酶D释放的9-kDa基质细胞SPARC片段在三阴性乳腺癌微环境中表现出促肿瘤活性。Bellengh [32] 等人发现在TNBC小鼠模型中，硬脂酰辅酶a去饱和酶SCD5驱动脂肪酸代谢重编程阻断SPARC的分泌，阻碍TNBC转移扩散并促进宿主免疫。Emmanuelle [30] 等人对148 名非转移性TNBC患者进行免疫组化研究，发现表达SPARC的CAF患者的无复发生存率显着较低。在TNBC中，SPARC由不同的CAF亚群表达。成纤维细胞分泌的SPARC通过抑制TNBC细胞粘附并刺激其运动和侵袭性而具有促肿瘤作用。总体而言，CAF中的SPARC表达是TNBC不良预后的独立预后标志。

5. 基于代谢物质的预后标志物

5.1. 铜代谢

血清铜水平有助于预测早期TNBC患者的生存情况 [33] 。铜诱导的氧化应激可以破坏DNA链或修改分子结构以激活癌基因 [34] 。最新的研究揭示了一种以前未知的细胞死亡调节机制，它被命名为铜死亡。铜死亡是通过铜与三羧酸(TCA)循环中的脂酰化酶结合而发生，导致随后的蛋白质聚集以及蛋白毒性应激，并最终导致细胞死亡 [35] 。Sha等 [36] 分析了TNBC患者预后与铜死亡相关基因表达水平之间的关联，发现ATP7A、DLST和LIAS的高表达水平与较差的总生存期(OS)相关，而LIPT1和PDHA1的高表达水平表明预后良好。

5.2. 铁代谢

细胞内亚铁过多可由载体SLC40A1挤出到细胞外空间，在那里它被转换回Fe3+，以平衡氧化还原状态和铁稳态。而铁积累过多会导致铁代谢紊乱和铁死亡，进而造成组成性氧化应激和器官损伤 [37] [38] 。Yuan [39] 等人在比较TNBC肿瘤和健康组织样本时，有87个铁死亡相关基因的差异表达(87/259, 33.59%)。其中七个基因(CA9, CISD1, STEAP3, HMOX1, DUSP1, TAZ, HBA1)与TNBC患者的总生存期显著相关，并确定了与预后相关的CISD1和STEAP3基因。预后风险评分值与CD4+T细胞浸润(P = 0.001)和髓系树突状细胞(P = 0.004)呈正相关。进一步的证据表明，STEAP3与TNBC患者OS有很强的特异性相关性(P < 0.05)。

6. 结语

随着生物医学技术的发展以及组学的兴起，会出现越来越多精准高效的预后生物标志物。我们需要全面了解TNBC的生态微环境，包括肿内微生物菌群、肿内代谢途径以及相关信号分子等，以此更深入剖析高度异质性肿瘤背后的奥秘。同样对于同一肿瘤的不同患者，需要深入了解个体差异带来的影响，这样我们才能够找到指导个体治疗的预后生物标志物。

文章引用

孙启航,贾存东. 三阴性乳腺癌预后标志物的研究进展
Progress in Prognostic Markers for Triple-Negative Breast Cancer[J]. 临床医学进展, 2023, 13(09): 15086-15091. https://doi.org/10.12677/ACM.2023.1392109

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    40. NOTES

    *通讯作者。

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