Research progress on relationship between interleukin-1 family and preeclampsia
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摘要: 白细胞介素(IL)-1家族细胞因子在多种组织和细胞中均可表达, 可通过多种信号通路参与多种疾病的发生与发展，主要功能是在炎症或免疫反应中调节免疫细胞的生长、分化和激活，并参与机体的多种生理及病理反应。IL-1家族有11个成员，其中绝大多数是促炎细胞因子，主要通过刺激炎症和自身免疫疾病相关基因的表达，在免疫调节及炎症进程中扮演着重要的角色。近年来，越来越多的研究报道了IL-1家族成员在子痫前期中的作用，本研究对IL-1家族细胞因子在子痫前期中的研究进展进行综述，以期为子痫前期的诊治提供新思路。Abstract: Interleukin (IL)-1 family cytokines can be expressed in many tissues and cells and participate in the occurrence and development of many diseases through multiple signaling pathways, and their main functions are to regulate the growth, differentiation and activation of immune cells in the inflammatory or immune response as well as participate in many physiological and pathological responses of the body. IL-1 family has 11 members, most of which are proinflammatory cytokines. These cytokines play important roles in immune regulation and inflammatory process by stimulating the expression of genes related to inflammation and autoimmune diseases. In recent years, more and more studies have reported the role of IL-1 family members in preeclampsia. This study reviewed the research progress of IL-1 family cytokines in preeclampsia, in order to provide new ideas for the diagnosis and treatment of preeclampsia.
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Keywords:
- interleukin /
- preeclampsia /
- immunity /
- cytokines /
- pathological reaction
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口腔鳞状细胞癌(OSCC)约占所有头颈部肿瘤的90%, 是全球重要的公共卫生问题[1]。尽管包括外科手术、放化疗在内的治疗策略大大优化，但OSCC患者总体5年生存率仍低于60%[2]。顺铂(DDP)化疗是晚期OSCC患者局部治疗的重要组成部分，可显著提高生存率，但70%~80%的复发患者表现出对DDP的耐药性[3]。长链非编码RNA(lncRNA)是一类内源性非编码RNA, 通过在表观遗传、转录前、转录后水平调控基因表达多种细胞过程中发挥作用。目前，多种lncRNA已被证实可通过抑制细胞增殖和迁移、促进细胞凋亡增加DDP耐药细胞系对DDP的敏感性[4-5]。长链非编码RNA01139(LINC01139)是一种肿瘤相关lncRNA, 肝癌中LINC01139表达上调，敲减LINC01139可抑制肝癌细胞恶性生物学行为[6]。生物信息学分析发现, LINC01139可能与微小RNA-300(miR-300)存在相互作用。研究[7]证实, miR-300-5p高表达可降低卵巢癌细胞的DDP耐药性，但LINC01139是否通过靶向调控miR-300表达影响OSCC细胞的DDP耐药性尚未可知。本研究探讨LINC01139、miR-300对DDP耐药OSCC细胞增殖、迁移和侵袭的影响以及分子机制，以期为OSCC化疗提供有效靶点。
1. 材料与方法
1.1 实验材料
CAL-27细胞购于美国模式培养物保藏中心; DDP(纯度≥99.9%)、噻唑蓝(MTT)试剂盒购于美国Sigma公司; LINC01139小干扰RNA(si-LINC01139) 及其阴性对照(si-NC)、LINC01139过表达载体(pcDNA-LINC01139)、质粒空载体(pcDNA)、miR-300模拟物(miR-300 mimics)及其阴性对照(miR-NC)、miR-300抑制物(anti-miR-300)及其阴性对照(anti-miR-NC)和聚合酶链反应(PCR)引物均由上海吉玛制药公司提供; LipofectamineTM 2000购自美国Invitrogen公司; Transwell小室、基质胶购于美国BD公司; 兔源细胞周期素D1(CyclinD1)、p21、基质金属蛋白酶-2(MMP-2)、基质金属蛋白酶-9(MMP-9)、甘油醛-3-磷酸脱氢酶(GAPDH)抗体以及山羊抗兔二抗购于上海艾博抗公司。
1.2 细胞培养、药物处理
参照文献[8]建立口腔鳞癌DDP耐药细胞株(CAL-27/DDP)。将对数期CAL-27细胞、CAL-27/DDP分别接种96孔板，当细胞贴壁后，分别加入终浓度为0.125、0.25、0.5、1、2、4、8 μg/mL的DDP并干预处理48 h, 采用MTT实验检测细胞增殖抑制率。
1.3 实验分组
将对数期CAL-27/DDP分为DDP+si-NC(转染si-NC)组、DDP+si-LINC01139(转染si-LINC01139)组、DDP+miR-NC(转染miR-NC)组、DDP+miR-300(转染miR-300 mimics)组、DDP+ si-LINC01139+anti-miR-NC(转染si-LINC01139和anti-miR-NC)组、DDP+si-LINC01139+anti-miR-300组(转染si-LINC01139和anti-miR-300)。以上各组在转染后均采用0.25 μg/mL的DDP干预处理48 h。将pcDNA-LINC01139、pcDNA、si-LINC01139、si-NC转染至细胞中，记为pcDNA-LINC01139组、pcDNA组、si-LINC01139组、si-NC组，使用实时荧光定量PCR(qRT-PCR)检测miR-300表达情况。细胞转染参照脂质体转染试剂LipofectamineTM 2000说明书进行。
1.4 qRT-PCR检测LINC01139和miR-300表达
收集CAL-27细胞和各组CAL-27/DDP, 以Trizol法提取细胞总RNA, 采用逆转录试剂盒合成cDNA, 采用SYBR Green Mix试剂进行qRT-PCR反应[9]。采用2-△△Ct法检测LINC01139和miR-300表达水平。
1.5 MTT法检测细胞增殖抑制率
收集各组CAL-27/DDP细胞，按照1×104个/孔接种到96孔板, 24 h后每孔加入20 μL的MTT试剂，培养箱孵育4 h, 弃去上清液，加入150 μL的DMSO, 振荡10 min溶解后，酶标仪测定490 nm波长处的光密度(OD)值[10-11]。
1.6 Transwell实验检测细胞迁移和侵袭
细胞迁移: 收集各组CAL-27/DDP细胞，采用无血清DMEM将培养基调整为5×104个/mL的单细胞悬液。取200 μL细胞悬液、500 μL含10%胎牛血清的DMEM培养基分别加入Transwell上室、24孔板下室。细胞培养箱孵育24 h, 棉拭子擦去上室内未穿膜细胞，甲醇固定20 min, 结晶紫染色10 min, 倒置随机选择5个视野计数、拍照，取均值[12-13]。细胞侵袭: 采用均匀包被基质胶的Transwell小室，实验前30 min水化后备用。
1.7 Western blot检测CyclinD1、p21、MMP-2和MMP-9蛋白表达
细胞裂解缓冲液提取各组CAL-27/DDP总蛋白, Nanodrop 2000测定蛋白浓度。十二烷基硫酸钠-聚丙烯酰胺凝胶电泳分离蛋白，并转移到聚偏二氟乙烯膜。将膜置于5%的脱脂牛奶中封闭后，稀释的一抗溶液室温孵育膜2 h, 稀释的二抗溶液室温孵育膜2 h, 增强型化学发光显色试剂盒暗室显色。目的蛋白表达水平采用灰度值与内参GAPDH灰度值比值表示。
1.8 双荧光素酶报告基因实验
将野生型/突变型(WT/MUT)LINC01139序列连接到PmirGLO双荧光素酶表达载体以构建WT/MUT-LINC01139, 该步骤由北京华大基因公司完成。利用Lipofectamine 2000将WT-LINC01139、MUT-LINC01139分别与miR-300(miR-300 mimics)、miR-NC共转染至CAL-27/DDP, 转染48 h收集细胞，根据双荧光素酶检测试剂盒进行荧光素酶活性测定。同时将pcDNA、pcDNA-LINC01139、si-NC、si-LINC01139分别转染CAL-27/DDP, 48 h后测定各组细胞miR-300表达水平。
1.9 统计学分析
每组设置3个平行实验，重复3次，所有数据均以均数±标准差表示。采用SPSS 17.0软件进行统计分析, 2组间比较采用t检验，多组间比较采用单因素方差分析，进一步组内两两比较采用SNK-q检验。P＜0.05为差异有统计学意义。
2. 结果
2.1 DDP对CAL-27细胞和CAL-27/DDP增殖抑制率的影响
与CAL-27比较，同一DDP浓度对CAL-27/DDP的抑制率较低, CAL-27/DDP的IC50值升高，差异有统计学意义(P＜0.05), 见表 1。
表 1 顺铂对CAL-27细胞和CAL-27/DDP增殖抑制率的影响(x±s)细胞 DDP浓度 IC50/(μg/mL) 0.125 μg/mL 0.25 μg/mL 0.5 μg/mL 1 μg/mL 2 μg/mL 4 μg/mL 8 μg/mL CAL-27(n=9) 11.32±1.14 22.45±2.27 34.62±3.55 45.86±4.31 59.33±5.12 73.21±7.56 86.22±8.13 1.17±0.19 CAL-27/DDP(n=9) 3.41±0.35* 7.11±0.72* 13.24±1.25* 19.83±1.74* 31.02±3.17* 39.65±3.88* 53.14±5.28* 6.65±0.51* CAL-27: 口腔鳞癌细胞; CAL-27/DDP: 口腔鳞癌顺铂耐药细胞; DDP: 顺铂。与CAL-27细胞比较, * P＜0.05。 2.2 CAL-27、CAL-27/DDP中LINC01139和miR-300的表达
与CAL-27比较, CAL-27/DDP中LINC01139的表达升高, miR-300的表达降低，差异有统计学意义(P＜0.05), 见表 2。
表 2 LINC01139和miR-300在CAL-27细胞和CAL-27/DDP细胞中的表达(x±s)细胞 LINC01139 miR-300 CAL-27(n=9) 1.00±0.06 1.00±0.05 CAL-27/DDP(n=9) 2.93±0.27* 0.34±0.03* LINC01139: 长链非编码RNA01139; miR-300: 微小RNA-300; CAL-27: 口腔鳞癌细胞; CAL-27/DDP: 口腔鳞癌顺铂耐药细胞。与CAL-27细胞比较, * P＜0.05。 2.3 抑制LINC01139表达联合DDP(0.25 μg/mL)对CAL-27/DDP细胞增殖、迁移和侵袭的影响
与DDP+si-NC组比较, DDP+si-LINC01139组CAL-27/DDP中LINC01139表达降低，增殖抑制率和p21蛋白表达升高，迁移和侵袭细胞数、CyclinD1、MMP-2和MMP-9蛋白表达降低，差异有统计学意义(P＜0.05), 见表 3、图 1。
表 3 抑制LINC01139表达联合DDP对CAL-27/DDP细胞增殖、迁移和侵袭的影响(x±s)组别 LINC01139 抑制率/% 迁移细胞数/个 侵袭细胞数/个 CyclinD1蛋白 p21蛋白 MMP-2蛋白 MMP-9蛋白 DDP+si-NC组(n=9) 1.00±0.08 6.41±0.63 105.23±10.22 88.14±8.42 0.61±0.06 0.33±0.03 0.72±0.07 0.66±0.06 DDP+si-LINC01139组(n=9) 0.51±0.05* 42.15±4.13* 56.39±5.21* 41.65±4.55* 0.20±0.02* 0.79±0.07* 0.30±0.03* 0.27±0.03* LINC01139: 长链非编码RNA01139; CyclinD1: 兔源细胞周期素D1; MMP-2: 基质金属蛋白酶-2; MMP-9: 基质金属蛋白酶-9。与DDP+si-NC组比较, * P＜0.05。 2.4 miR-300过表达联合DDP(0.25 μg/mL)对CAL-27/DDP细胞增殖、迁移和侵袭的影响
与DDP+miR-NC组比较, DDP+miR-300组CAL-27/DDP中miR-300表达显著升高，增殖抑制率和p21蛋白表达升高，迁移和侵袭细胞数、CyclinD1、MMP-2和MMP-9蛋白表达降低，差异有统计学意义(P＜0.05), 见表 4和图 2。
表 4 miR-300过表达联合DDP对CAL-27/DDP细胞增殖、迁移和侵袭的影响(x±s)组别 miR-300 抑制率/% 迁移细胞数/个 侵袭细胞数/个 CyclinD1蛋白 p21蛋白 MMP-2蛋白 MMP-9蛋白 DDP+miR-NC组(n=9) 1.00±0.06 7.12±0.77 101.25±9.84 86.14±8.63 0.63±0.06 0.32±0.03 0.71±0.07 0.68±0.06 DDP+miR-300组(n=9) 2.57±0.24* 35.48±3.55* 60.55±6.31* 53.47±5.33* 0.28±0.03* 0.75±0.07* 0.37±0.03* 0.30±0.03* miR-300: 微小RNA-300; CyclinD1: 兔源细胞周期素D1; MMP-2: 基质金属蛋白酶-2; MMP-9: 基质金属蛋白酶-9。与DDP+miR-NC组比较, * P＜0.05。 2.5 LINC01139靶向调控miR-300的表达
靶基因预测工具LncBase Predicted v. 2分析显示, LINC01139与miR-300存在特异性结合的核苷酸序列，见图 3。miR-300 mimics和WT-LINC01139共转染CAL-27/DDP细胞荧光素酶活性较miR-NC和WT-LINC01139共转染细胞降低，差异有统计学意义(P＜0.05); miR-300 mimics和MUT-LINC01139共转染CAL-27/DDP细胞荧光素酶活性与miR-NC和MUT-LINC01139共转染细胞比较，差异无统计学意义(P>0.05), 见表 5。pcDNA-LINC01139组CAL-27/DDP细胞miR-300表达较pcDNA组降低, si-LINC01139组CAL-27/DDP细胞miR-300表达较si-NC组升高，差异有统计学意义(P＜0.05), 见表 6。
表 5 双荧光素酶报告实验(x±s)组别 WT-LINC01139 MUT-LINC01139 miR-NC组(n=9) 1.00±0.06 1.02±0.08 miR-300组(n=9) 0.57±0.05* 0.99±0.07 与miR-NC组比较, * P＜0.05。 表 6 LINC01139调控miR-300的表达(x±s)组别 miR-300 pcDNA组(n=9) 1.00±0.07 pcDNA-LINC01139组(n=9) 0.53±0.05* si-NC组(n=9) 1.02±0.06 si-LINC01139组(n=9) 2.68±0.27# F 381.236 P ＜0.001 与pcDNA组比较, * P＜0.05; 与si-NC组比较, #P＜0.05。 2.6 干扰miR-300表达逆转了抑制LINC01139表达对CAL-27/DDP细胞DDP耐药性的作用
与DDP+si-NC组比较, DDP+si-LINC01139组CAL-27/DDP中miR-300表达显著升高，增殖抑制率、p21蛋白表达显著升高，迁移和侵袭细胞数、CyclinD1、MMP-2和MMP-9蛋白表达显著降低; 与DDP+si-LINC01139+anti-miR-NC组比较, DDP+si-LINC01139 +anti-miR-300组CAL-27/DDP中miR-300表达显著降低，增殖抑制率、p21蛋白表达显著降低，迁移和侵袭细胞数、CyclinD1、MMP-2和MMP-9蛋白表达显著升高(P＜0.05)。见表 7和图 4。
表 7 干扰miR-300表达逆转了抑制LINC01139表达对CAL-27/DDP细胞DDP耐药性的作用(x±s)组别 miR-300 抑制率/% 迁移细胞数/个 侵袭细胞数/个 CyclinD1蛋白 p21蛋白 MMP-2蛋白 MMP-9蛋白 DDP+si-NC组(n=9) 1.00±0.08 7.06±0.71 106.24±9.56 85.14±8.36 0.62±0.06 0.31±0.03 0.73±0.07 0.67±0.06 DDP+si-LINC01139组(n=9) 2.84±0.27* 43.25±4.31* 57.14±5.33* 43.51±4.33* 0.22±0.03* 0.77±0.07* 0.33±0.03* 0.29±0.03* DDP+si-LINC01139+anti-miR-NC组(n=9) 2.86±0.28 44.69±4.52 55.86±5.52 42.69±4.74 0.21±0.02 0.78±0.06 0.32±0.03 0.28±0.02 DDP+si-LINC01139+anti-miR-300组(n=9) 1.53±0.15# 21.36±2.54# 83.47±8.35# 69.71±6.33# 0.51±0.05# 0.40±0.04# 0.64±0.06# 0.56±0.05# miR-300: 微小RNA-300; CyclinD1: 兔源细胞周期素D1; MMP-2: 基质金属蛋白酶-2; MMP-9: 基质金属蛋白酶-9。
与DDP+si-NC组比较, * P＜0.05; 与DDP+si-LINC01139+anti-miR-NC组比较, #P＜0.05。3. 讨论
近年来研究[15]发现, lncRNA在OSCC耐药过程中起着重要的作用。lncRNA浆细胞瘤转化迁移基因1( PVT1 )在DDP耐药组织和细胞系中经常被上调，并且与较差的总体生存密切相关。在DDP耐药OSCC细胞中同源框基因11反义RNA( HOXA11-AS )亦表达上调，敲减 HOXA11-AS 能够降低DDP耐药OSCC细胞的增殖，增加DDP诱导的细胞毒性，抑制小鼠移植瘤的生长，为改善OSCC化疗提供了潜在靶点[16]。干扰HOX转录反义RNA(HOTAIR)表达可抑制OSCC细胞自噬，促进细胞凋亡，增加对DDP的敏感性[17]。本研究发现, OSCC的DDP耐药细胞株CAL-27/DDP中LINC01139表达升高，提示LINC01139异常表达可能与OSCC DDP耐药有关。功能分析发现，抑制LINC01139表达可降低CAL-27/DDP的增殖、迁移和侵袭能力。p21是细胞周期的负调控因子，通过与CyclinD1、细胞周期依赖性激酶(CDKs)、CyclinD1/CDKs复合物结合导致细胞周期阻滞，阻断细胞增殖过程[18]。MMP-2和MMP-9是MMPs家族的重要成员，几乎能够降解细胞外基质中所有蛋白成分，改变细胞间黏附，破坏肿瘤细胞侵袭转移的组织学屏障[19]。本研究发现，抑制LINC01139表达后CAL-27/DDP中CyclinD1、MMP-2和MMP-9表达水平降低, p21表达水平升高，提示LINC01139在CAL-27/DDP增殖、迁移和侵袭中发挥促进作用。
lncRNA与miRNA的相互作用是调控肿瘤生物学功能的重要机制[20-21]。本研究发现miR-300为LINC01139下游候选靶点。miR-300的异常表达已被报道参与OSCC的发生和发展, OSCC患者miR-300水平降低，过表达miR-300可抑制OSCC细胞的增殖、侵袭和上皮间质转化过程[22]。miR-300通过靶向淋巴样增强子结合因子1调节肝细胞癌的生长和转移[23]。lncRNA牛磺酸上调基因1(TUG1)通过负调控miR-300促进胆囊癌细胞增殖和转移[24]。本研究显示, miR-300在CAL-27/DDP中表达降低，过表达miR-300可促进CAL-27/DDP的增殖、迁移和侵袭，促进p21表达，抑制CyclinD1、MMP-2和MMP-9表达水平。进一步实验显示, LINC01139对miR-300表达具有靶向负调控作用，且干扰miR-300表达能够逆转抑制LINC01139表达对CAL-27/DDP细胞的增殖、迁移和侵袭抑制作用。因此, LINC01139/miR-300分子轴在OSCC的DDP耐药中发挥重要作用。
总之，本研究发现LINC01139能够促进OSCC的DDP耐药性，抑制LINC01139可通过上调miR-300达到抑制CAL-27/DDP细胞增殖、迁移和侵袭的目的，为改善OSCC化疗提供了潜在靶点。
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