lncRNA PSMA3-AS1 靶向 miR-3619-5p 调控宫颈癌 SiHa 细胞增殖、迁移及侵袭的分子机制研究

目的 探讨 lncRNA PSMA3-AS1 调控宫颈癌细胞增殖、 迁移及侵袭的分子机制。 方法 收集 2020 年 3 月至 2021 年 6 月西安医学院第二附属医院收治的 42 例宫颈癌患者的癌组织及其癌旁组织标本, 采用 qRT-PCR 法检测宫颈癌组织、 癌旁组织、 人宫颈上皮永生化细胞 H8、 与人宫颈癌细胞系 SiHa、 HeLa、 Caski 中 lncRNA PSMA3-AS1、 miR-3619-5p 的表达量; 以 SiHa 细胞为研究对象, 分组为: si-NC 组、 si-lncRNA PSMA3-AS1 组、 miR-NC 组、 miR-3619-5p 组、 anti-miR-NC + si-lncRNA PSMA3-AS1 组、 anti-miR-3619-5p + si-lncRNA PSMA3-AS1 组; MTT 法与 Transwells 实验分别检测每组 SiHa 细胞的增殖活力、 迁移及侵袭能力; 双 荧光素酶报告实验检测 miR-3619-5p 过表达对野生型载体 lncRNA PSMA3-AS1-WT、 突变型载体 lncRNA PSMA3-AS1-MUT 荧光素酶活性的影响; Western 印迹检测 MMP2、 MMP9 蛋白表达量。 结果 宫颈癌组织中 lncRNA PSMA3-AS1 的表达量比癌旁组织增加 ( P < 0. 01), miR-3619-5p 的表达量比癌旁组织减少 ( P < 0. 01); 与 H8 细胞比较, SiHa、 HeLa、 Caski 细胞中 lncRNA PSMA3-AS1 的表达量升高 (P< 0. 01), miR-3619-5p 的表达量降低 (P< 0. 01); 与 si-NC 组比较, si-lncRNA PSMA3-AS1 组细胞活力和 MMP2、 MMP9 蛋 白水平降低 (P< 0. 05), 迁移及侵袭细胞数减少 (P< 0. 05); 与 miR-NC 组比较, miR-3619-5p 组细胞活力 和 MMP2、 MMP9 蛋白水平降低 (P< 0. 01), 迁移及侵袭细胞数减少 (P< 0. 05); miR-3619-5p 过表达可抑 制 lncRNA PSMA3-AS1-WT 的荧光素酶活性 (P< 0. 01), 而未能影响 lncRNA PSMA3-AS1-MUT 的荧光素酶活 性; 与 anti-miR-NC + si-lncRNA PSMA3-AS1 组比较, anti-miR-3619-5p + si-lncRNA PSMA3-AS1 组细胞活力和 MMP2、 MMP9 蛋白水平升高 (P< 0. 01), 迁移及侵袭细胞数增多 (P< 0. 01)。 结论 干扰 lncRNA PSMA3- AS1 表达可通过促进 miR-3619-5p 而降低宫颈癌细胞增殖、 迁移及侵袭能力。     

lncRNA CERS6-AS1 通过调控 miR-138-2-3p 抑制人胶质瘤细胞系增殖

目的 探讨 lncRNA CERS6-AS1 对胶质瘤细胞生物学行为的影响及其可能作用机制。 方法 qRT-PCR 法检测胶质瘤组织、 癌旁组织中 CERS6-AS1 和 miR-138-2-3p 的表达量; Pearson 法分析胶质瘤组织中 CERS6-AS1 与 miR-138-2-3p 表达量的相关性; 体外培养人胶质瘤细胞 T98G, 将 si-NC、 si-CERS6-AS1、 miR-NC、 miR-138-2-3p mimics、 si-CERS6-AS1 与 anti-miR-NC、 si-CERS6-AS1 与 anti-miR-138-2-3p 分 别 转 染 至 T98G 细胞; CCK-8 法、 平板克隆形成实验、 Transwell 小室实验分别检测细胞增殖、 克隆形成、 迁移及侵袭 能力; 双荧光素酶报告基因实验检测 CERS6-AS1 和 miR-138-2-3p 的靶向关系。 结果 与癌旁组织比较, 胶 质瘤组织中 CERS6-AS1 的表达量升高 (P< 0. 05), miR-138-2-3p 的表达量降低 (P< 0. 05); CERS6-AS1 与 miR-138-2-3p 呈负相关 (r = - 0. 8899, P< 0. 001); si-CERS6-AS1 组细胞活力、 克隆形成细胞数、 迁移及侵 袭细胞数均低于 si-NC 组 (P< 0. 05); CERS6-AS1 可靶向调节 miR-138-2-3p 的表达; miR-138-2-3p 组细胞活 力、 克隆形成细胞数、 迁移及侵袭细胞数均少于 miR-NC 组 (P< 0. 05); si-CERS6-AS1 + anti-miR-138-2-3p 组细胞活力、 克隆形成细胞数、 迁移及侵袭细胞数均比 si-CERS6-AS1 + anti-miR-NC 组增多 (P< 0. 05)。 结论 干扰 CERS6-AS1 表达可通过调控 miR-138-2-3p 而抑制胶质瘤细胞增殖、 克隆形成、 迁移及侵袭。     

Long non-coding RNA DLGAP1-AS1 promotes the progression of gastric cancer via miR-515-5p/MARK4 axis

Long non-coding RNA (lncRNA) is an essential regulator of carcinogenesis and cancer progression. In the study, we explored the role of lncRNA DLGAP1-AS1 in gastric cancer (GC). qRT-PCR was carried out to detect DLGAP1-AS1 expression in GC tissues and cell lines. CCK-8 assay, EdU assay, and transwell experiments were employed to detect the malignant biological behaviors of GC cells with DLGAP1-AS1 knockdown or overexpression. Bioinformatics and dual-luciferase report assay were used to confirm the binding relationship between DLGAP1-AS1 and miR-515-5p. MARK4 expression was detected by western blot after DLGAP1-AS1/miR-515-5p was selectively regulated. DLGAP1-AS1 was up-regulated in GC tissues and cell lines, and its high expression was closely associated with larger tumor size, higher TNM stage, and lymph node metastasis. Furthermore, DLGAP1-AS1 overexpression enhanced cell proliferation, migration, and invasion, and miR-515-5p could reverse these effects. DLGAP1-AS1 participated in the regulation of the MARK4 signaling pathway by targeting miR-515-5p. DLGAP1-AS1 promoted GC progression through miR-515-5p/MARK4 signaling pathway.     

LncRNA TP73-AS1 accelerates tumor progression in gastric cancer through regulating miR-194-5p/SDAD1 axis

Background

Long noncoding RNAs (lncRNAs) have been considered as significant regulators in many cancer progression, such as proliferation, invasion and other path of evolution. Nevertheless, we have not had a grasp of the role of lncRNA TP73-AS1 in gastric cancer (GC).

miR-142-5p regulates pancreatic cancer cell proliferation and apoptosis by regulation of RAP1A

Pancreatic cancer, one of the fatal and aggressive malignancies, leads the sixth cancer-associated death in China. microRNAs are believed to exert function in the diagnosis and treatment of pancreatic cancer. In the present study, we firstly found that miR-142-5p was downregulated in pancreatic cancer tumor tissues while Ras-related protein Rap-1 A (RAP1A) was upregulated compared with para-carcinoma non-tumor tissues. Then, we found that RAP1A could be a putative target gene of miR-142-5p by bioinformatics tool TargetScan. Furthermore, we conducted luciferase reporter assay, RT-qPCR, western blot and correlation analysis to demonstrate that miR-142-5p could negatively regulate RAP1A expression by binding to its 3′UTR. In addition, cell-counting kit 8 (CCK-8) and flow cytometry assays certified that miR-142-5p overexpression may inhibit pancreatic cancer cell proliferation but promote cell apoptosis; while the variation could be reversed by co-transfected with pcDNA3.1-RAP1A. Finally, miR-142-5p overexpression downregulated p-ERK1/2, phosphate p38 mitogen-activated protein kinases (p-p38); however, the variation induced by miR-142-5p mimic could be reversed by co-transfected with pcDNA3.1-RAP1A. In conclusion, our findings indicate that targeting miR-142-5p may provide a novel strategy for the treatment of pancreatic cancer.     

miR-219-5p对非小细胞肺癌细胞增殖、凋亡与侵袭的影响及其机制

目的:探索miR-219-5p对非小细胞肺癌(non-small cell lung cancer,NSCLC)细胞增殖、凋亡及侵袭的影响,并探讨其机制.方法:采用RT-PCR检测miR-219-5p在NSCLC细胞系H1299,A549,H1975及正常肺上皮细胞系BEAS-2B中的表达.将NSCLC细胞系H1299分成对照组和miR-219-5p组,用Lipofectamine 2000分别转染miR-219-5p scramble和miR-219-5p mimics,采用MTT法、流式细胞术及Transwell实验分别检测比较两组细胞增殖、凋亡及侵袭能力,Western印迹测定表皮生长因子受体(epidermal growth factor receptor,EGFR)及裂解型多聚腺苷二磷酸核糖聚合酶(poly ADP ribose polymerase,PARP)在两组细胞中的表达.结果:miR-219-5p在H1299,A549和H1975细胞系中的表达量均低于BEAS-2B,差异有统计学意义(P<0.05);MTT实验显示在48,72,96及120 h,miR-219-5p组OD490 nm值显著低于对照组,差异有统计学意义(P<0.05);miR-219-5p组细胞凋亡率显著高于对照组(13.33%±1.20%vs 3.43%±0.12%),差异有统计学意义(P<0.01);miR-219-5p组侵袭细胞数显著少于对照组(67.5±9.9 vs 189.5±16.7),差异有统计学意义(P<0.05);miR-219-5p组EGFR蛋白相对表达量为0.35±0.07,miR-219-5p组EGFR蛋白相对表达量显著低于对照组(1.0),差异有统计学意义(P<0.01);miR-219-5p组裂解型PARP蛋白相对表达量显著高于对照组(2.74±0.17 vs 1.0),差异有统计学意义(P<0.01).结论:miR-219-5p可抑制NSCLC的细胞增殖和侵袭并促进其凋亡,其机制可能与下调EGFR及上调PARP的表达有关.     

LncRNA NCK1-AS1 promotes non-small cell lung cancer progression via regulating miR-512-5p/p21 axis

ObjectiveThis study aimed at probing into the effect of lncRNA NCK1-AS1 on proliferation, migration and invasion of non-small cell lung cancer (NSCLC) cells and its regulatory function on miR-512-5p/p21 molecular axis.MethodsQuantitative real-time polymerase chain reaction (qRT-PCR) was used to assess the expressions of NCK1-AS1 and miR-512-5p in NSCLC tissues and cell lines. The alterations of cell proliferation, migration, invasion and cell cycle were examined by cell counting kit-8 (CCK-8) assay, BrdU experiment, Transwell experiment and flow cytometry, respectively. The dual-luciferase reporter assay and RNA immunoprecipitation experiment were performed to validate the binding relationships between miR-512-5p and NCK1-AS1, and miR-512-5p the 3'UTR of p21 mRNA. Western blot was used to determine the effects of NCK1-AS1 and miR-512-5p on p21 protein expression.ResultsNCK1-AS1 expression was up-regulated in NSCLC tissues and cells, and its high expression was correlated with shorter overall survival time and faster progression of patients. Overexpression of NCK1-AS1 promoted NSCLC cell proliferation, migration and invasion, and accelerated the cell cycle, whereas NCK1-AS1 siRNA inhibited these malignant biological behaviors, and arrested cell cycle. NCK1-AS1 could bind to miR-512-5p, p21 was verified as a target gene of miR-512-5p, and NCK1-AS1 could up-regulate the expression of p21 in NSCLC cells via repressing miR-512-5p expression.ConclusionNCK1-AS1 promotes NSCLC progression by regulating miR-512-5p/p21 molecular axis.     

LncRNA UNC5B-AS1靶向miR-339-5p调控人肺腺癌细胞系A549增殖和凋亡

目的 旨在研究lncRNA UNC5B-AS1靶向miR-339-5p对肺癌细胞增殖和凋亡的影响及分子机制.方法 体外培养人肺腺癌细胞系A549;将si-NC、si-UNC5B-AS1、miR-NC、miR-339-5p mimics、si-UNC5B-AS1与anti-miR-NC、si-UNC5B-AS1与anti...     

Cyclic RNA Circ_0000735 sponges miR-502-5p to promote bladder cancer cell proliferation and invasion and inhibit apoptosis

Objective: The objective of this study was to investigate the effect on the proliferation, invasion, and apoptosis of bladder cancer cells through miR-502-5p of the Circ_0000735 circular RNA. Methods: Circ_0000735 and miR-502-5p expression of bladder cancer patients in malignant and paracancerous tissues was identified using qRT-PCR. Nucleoplasm isolation assay and RNase R enzymatic assay were used to classify Circ_0000735 subcellular origin and stability. Dual luciferase reporter assay and RIP assay were used to confirm Circ_0000735 and miR-502-5p targeting relationships. Cell proliferation, apoptosis, and invasion capacity were identified using CCK8, flow cytometry, and transwell assays. To confirm the effect of Circ_0000735 on tumorigenesis in nude mice, in vivo experiments were conducted. Results: Circ_0000735 expression was increased in bladder cancer tissues and cells compared with paraneoplastic tissues and normal cells, and miR-502-5p expression was reduced (both P<0.05). In the cytoplasm, Circ_0000735 was largely clustered and could not be digested by the RNase R enzyme, and ceRNA may play a role in bladder cancer cells. Circ_0000735 silencing prevented cell proliferation and invasion and facilitated apoptosis (all P<0.05). The incorporation of miR-502-5p inhibitor rescued the effect on bladder cancer cells of Circ_0000735 silencing. In vitro experiments showed that inhibition of Circ_0000735 expression was beneficial in suppressing tumorigenic ability in nude mice. Conclusion: Circ_0000735 can adsorb miR-502-5p to promote bladder cancer cell proliferation and invasion and inhibit apoptosis. Circ_0000735 may be an effective molecular target for bladder cancer therapy.     

LncRNA HEIH通过miR-98-5p调节肺癌细胞增殖和凋亡

目的探讨lncRNA HEIH对肺癌细胞增殖和凋亡的影响及其作用机制。方法培养人正常肺上皮细胞BEAS-2B和肺癌细胞系A549、A427、H1299和TKB-1,RT-qPCR检测细胞中HEIH表达水平;分别转染si-HEIH和miR-98-5p mimics至A549细胞,沉默A549细胞中HEIH表达或过表达miR-98-5p;MTT法检测细胞增殖;流式细胞仪检测细胞凋亡;Western blot检测CCND1、caspase-3、SHH、GLI-1、PTCH和SUFU蛋白表达。双荧光素酶报告基因实验验证HEIH与miR-98-5p之间的关系。结果与正常肺上皮细胞BEAS-2B相比,肺癌细胞系A549、A427、H1299和TKB-1中HEIH表达水平显著升高(P<0.05).其中A549细胞中的HEIH表达最高。因此,后续实验选择A549细胞为研究对象。沉默HEIH表达或过表达miR-98-5p均可降低A549细胞培养12、48和72 h后吸光度值(A值)(P<0.05)(MTT法);升高凋亡率(P<0.05);抑制CCND1蛋白表达(P<0.05),促进caspase-3蛋白表达(P<0.05)。并且过表达miR-98-5p还抑制了A549细胞中SHH和GLI-1的mRNA和蛋白表达(P<0.05),促进了PTCH和SUFU的mRNA和蛋白表达水平(P<0.05)。过表达HEIH逆转了过表达miR-98-5p对A549细胞增殖、凋亡以及SHH、GLI-1、PTCH和SUFU的mRNA和蛋白表达的影响。结论沉默HEIH表达可能通过靶向miR-98-5p经Hedgehog信号通路抑制肺癌细胞的增殖,并促进其凋亡。     

DAAM1-mediated migration and invasion of ovarian cancer cells are suppressed by miR-208a-5p

Ovarian cancer (OvCa) has the highest morbidity among all gynecologic cancers worldwide, and its distant metastasis is one of main causes for the poor prognosis of OvCa patients. Our previous studies have reported that DAAM1-involved signaling pathways play vital roles in metastasis of breast cancer. However, whether DAAM1 participates in OvCa migration and/or invasion is still unknown. The impact of DAAM1 on cell migration and invasion in OvCa was evaluated by wound healing assay and Boyden chamber assay. The specific miRNA targeting DAAM1 was predicted by bioinformatics methods and verified by dual-luciferase activity assay. The miR-208a-5p expression levels in OvCa tissues and the impacts of miR-208a-5p on cell migration and invasion were also assessed, respectively. High expression of DAAM1 was associated with distant metastasis in OvCa. Silence of DAAM1 by siRNA blocked the migration and invasion of OVCAR-3 cells. MiR-208a-5p directly targeted DAAM1 and was shown a decreased expression in metastatic OvCa tissues. Elevated expression of miR-208a-5p inhibited the migration and invasion of OVCAR-3 cell which can be rescued by DAAM1 overexpression. Our data suggest that miR-208-5p/DAAM1 axis participates in OvCa migration and invasion and may be a novel clinical target to limit OvCa metastasis.     

宫颈癌组织miR-574-5p的表达及其下调后对宫颈癌SiHa细胞的影响

目的探讨宫颈癌患者组织中miR-574-5p的表达及其下调时对宫颈癌Si Ha细胞增殖、凋亡和迁移的影响。方法用实时荧光定量PCR测定80例宫颈癌组织中miR-574-5p水平。将miR-574-5p抑制物转染宫颈癌Si Ha细胞,四甲基偶氮唑盐比色法(MTT法)检测细胞增殖能力,流式细胞仪检测细胞凋亡率,Tanswell迁移实验检测细胞侵袭能力。结果宫颈癌组织中miR-574-5p相对表达水平高于正常宫颈组织(P0.05);高表达的miR-574-5p与肿块大小、临床分期、病理分级和淋巴结转移有关(P0.05);转染miR-574-5p抑制物组与空白组及阴性对照组相比,Si Ha细胞增殖能力下降(P0.05);细胞凋亡率明显增加(P0.05);转染后细胞穿膜能力明显减弱(P0.05)。结论 miR-574-5p的高表达与宫颈癌的进展有关,下调miR-574-5p的表达抑制了宫颈癌Si Ha细胞的增殖和迁移,促进其凋亡,有望成为宫颈癌基因治疗的靶点。     

miR-671-5p通过靶向肿瘤坏死因子α诱导蛋白8调控胰腺癌细胞增殖和凋亡

目的：探讨miR-671-5p 靶向肿瘤坏死因子α 诱导蛋白8（ TNFAIP8）对胰腺癌细胞增殖和凋亡的影响。 方法：实时荧光定量PCR（ qRT-PCR）和免疫印迹检测20 例胰腺癌组织和与其配对的癌旁正常组织miR-617-5p、 TNFAIP8 mRNA和TNFAIP8表达水平,验证miR-671-5p 和TNFAIP8的靶向调控关系。将体外培养胰腺癌细胞 capan-1分为miR-NC组、miR-671-5p 组、si-NC 组、si-TNFAIP8 组、miR-671-5p+pcDNA组和miR-671-5p+pcDNATNFAIP8 组。采用四甲基偶氮唑蓝（ MTT）实验检测细胞活力,流式细胞术检测细胞凋亡,免疫印迹检测细胞周 期蛋白D1（ cyclin D1）、p21、B细胞淋巴瘤/ 白血病-2（ Bcl-2）和Bcl-2 相关蛋白（ Bax）的表达水平。结果：与 癌旁正常组织比较,胰腺癌组织miR-617-5p 表达量显著降低,TNFAIP8 的表达量显著升高。miR-671-5p 靶向负向 调控TNFAIP8 表达。与miR-NC组比较,miR-671-5p 组capan-1 细胞活力显著降低,细胞凋亡率显著升高,cyclin D1和Bcl-2 的表达量显著降低,p21 和Bax 的表达量显著升高;与si-NC 组比较,si-TNFAIP8 组capan-1 细胞活力 显著降低,细胞凋亡率显著升高,cyclin D1和Bcl-2 表达量显著降低,p21 和Bax 表达量显著升高;与miR-671- 5p+pcDNA 组比较,miR-671-5p+pcDNA-TNFAIP8 组capan-1 细胞活力显著升高,细胞凋亡率显著降低,cyclin D1和Bcl-2 的表达量显著升高,p21 和Bax 的表达量显著降低。结论：miR-671-5p 通过靶向下调TNFAIP8 抑制胰 腺癌细胞增殖并促进其凋亡。上调miR-671-5p 是胰腺癌潜在治疗靶点。     

miR-593-5p inhibit cell proliferation by targeting PLK1 in non small cell lung cancer cells

Worldwide, lung cancer has the highest rates of mortality and morbidity, with the majority of its pathology attributable to non-small cell lung cancer (NSCLC). MicroRNAs are pivotal in the occurrence and development of cancer. However, the role of miRNA-593-5p in the progression of NSCLC is not clear. In this study, we investigate, in vitro, whether miRNA-593-5p inhibits NSCLC cell proliferation. To clarify its specific mechanism of inhibition, we used bioinformatics to predict its target genes and identified PLK1. Luciferase reporter assay confirmed the binding of miR-593-5p to the PLK1 3′-UTR in a sequence-specific manner in NSCLC cells. Additionally, we also found through Western blot and quantitative RT-PCR that miR-593-5p down-regulates the expression of PLK1 protein. Finally, PLK1 overexpression was shown to disinhibit NSCLC cell proliferation. Taken together, this evidence suggests that miR-593-5p inhibits NSCLC cell proliferation by inhibiting PLK1 expression.     

miR-32-5p靶向ZEB1、ZEB2基因调控乳腺癌增殖和侵袭能力的机制

目的 探讨ZEB1和ZEB2在乳腺癌中的作用及miR-32-5 p对乳腺癌调控的分子机制.方法 通过Western blot和qRT-PCR检测乳腺癌和癌旁组织中ZEB1、ZEB2和miR-32-5 p的表达,筛选出ZEB1和ZEB2高表达的乳腺癌细胞系,采用Western blot和qRT-PCR检测敲减效率.应用克...     

Ginsenoside Rh2 inhibits thyroid cancer cell migration and proliferation via activation of miR-524-5p

IntroductionThyroid cancer is an important disease that threatens the health of humans. Ginsenoside Rh2 is known as an anticancer molecule; however, its function in thyroid cancer cells has not been reported. In the present study, we identified that Rh2 treatment of the thyroid cancer cell line K1 inhibited cell migration and proliferation.Material and methodsWe determined the Rh2 function in thyroid cancer cell lines. By RT-PCR, expression of miR-524-5p and related genes were determined. The cell phenotype including cell migration and proliferation were detected after serials treatment. The relevant protein level were checked by Western blot.ResultsInterestingly, we observed that miR-524-5p, a type of miRNA, had lower expression in the thyroid cancer cell lines TPC-1, K1, and NPA than in the normal thyroid cell line Nthyri3-1. Additionally, Rh2 treatment induced miR-524-5p expression. Further examination using overexpression of miR-524-5p identified that the miR-524-5p mimic inhibited cell migration and proliferation of the K1 line. Similar to Rh2-treated cells, the miR-524-5p mimic-expressing cells had increased E-cadherin and reduced vimentin levels compared to the control cells. Next, we examined the relationship between Rh2 and miR-524-5p with respect to thyroid cell migration and proliferation. Treatment with Rh2 and miR-524-5p inhibitor suppressed Rh2 action on K1 thyroid cell migration and proliferation, and the rates were similar to those in control cells, suggesting that Rh2 might induce miR-524-5p expression to inhibit thyroid cancer cell migration and proliferation.ConclusionsOur analyses identified Rh2 and miR-524-5p action on thyroid cancer cell migration and proliferation as well as the linkage between Rh2 and miR-524-5p in thyroid cancer cell development.     

miR-1247-5p对Smad2基因的靶向调控作用

目的利用miR-1247-5p过表达模拟物mimics,研究miR-1247-5p对TGF-β信号通路中关键蛋白Smad2的靶向调控作用。方法合成模拟miR-1247-5p过表达的模拟物mimics,及抑制miR-1247-5p表达的抑制物inhibitors;同时构建与miR-1247-5p互补靶基因Smad2的3'非翻译区,将其克隆到线性化的Report荧光报告载体中。将测序鉴定阳性的report-Smad2 3'-UTR重组质粒,与miR-1247-5p的mimics/inhibitors共转染至HEK-293T细胞,通过relative luciferase activity实验验证靶向关系,并通过Western blot实验进一步检测Smad2蛋白表达水平。结果成功构建report-Smad2 3'-UTR重组质粒,Western blot实验表明转染miR-1247-5p mimics组中Smad2蛋白表达下调(P0.05);而转染miR-1247-5p inhibitors组中,Smad2蛋白表达上调(P0.05)。结论证实miR-1247-5p直接靶向TGF-β信号通路中关键蛋白Smad2的表达,在蛋白水平对其进行调控,为进一步研究miRNA在细胞通路中的调控作用提供了依据。