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1.
MicroRNAs are a class of small non-coding RNAs that play essential roles in cancer development and progression. Recent studies suggested that abnormal expression of miRNAs occurs frequently in non-small cell lung cancer (NSCLC) tissues compared to adjacent normal tissues. In this study, we investigated the expression and the biological roles of miR-106a in non-small cell lung cancer. Our results showed that miR-106a was up-regulated in NSCLC tissues and cell lines. Inhibition of miR-106a in NSCLC cells substantially inhibited cell proliferation, migration, and invasion. Phosphatase and tensin homolog (PTEN) was identified as a direct target of miR-106a, and over-expression of miR-106a suppressed PTEN by direct binding to its 3’-untranslated region (3’-UTR). Furthermore, the presence of miR-106a was inversely correlated with PTEN in NSCLC tissues. Overall, this study suggested that miR-106a inhibited the growth and metastasis of NSCLC cells by decreasing PTEN expression. These data provide novel insights with potential therapeutic applications for the treatment of NSCLC.  相似文献   

2.
Increasing evidence has shown that microRNAs play critical roles in the initiation and progression of non-small cell lung cancer (NSCLC). miR-185 is deregulated in various cancers, whereas its functional mechanism in NSCLC is still unclear. Here, we confirmed that the expression of miR-185 was significantly down-regulated in NSCLC tissues and cell lines. miR-185 over-expression caused significant suppression of in vitro cell proliferation, migration and invasion, and in vivo tumor growth. We subsequently identified that AKT1 was a target gene of miR-185. Re-expression of AKT1 could partially rescue the inhibitory effects of miR-185 on the capacity of NSCLC cell proliferation and motility. Collectively, we conclude that miR-185 has a critical function by blocking AKT1 in NSCLC cells, and it may be a novel therapeutic agent for miRNA based NSCLC therapy.  相似文献   

3.
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.  相似文献   

4.
MicroRNA-137 (miR-137) was reported to be dysregulated in several human cancers. However, the function and mechanism of miR-137 in non-small cell lung cancer (NSCLC) is still unclear. In the current study, we explored the role of miR-137 in NSCLC progression. Using qRT-PCR, our data showed that miR-137 was significantly down-regulated in NSCLC tissues and cell lines. In vitro functional assay, we found that over-expression of miR-137 suppressed NSCLC cells proliferation, migration and invasion, indicating that miR-137 could act as a tumor suppressor in NSCLC progression. In addition, bone morphogenetic protein-7 (BMP7) was identified as a target of miR-137 in NSCLC cells, Luciferase reporter assay suggested that miR-137 directly targeted 3’-UTR of BMP7, and correlation analysis revealed that BMP7 inversely correlated with miR-137 in NSCLC tissues. Furthermore, Restoration of BMP7 remarkably reversed the tumor suppressive effects of miR-137 on NSCLC cell proliferation, migration, and invasion. Taken together, our findings suggested that miR-137/BMP7 axis could contribute to the progression of NSCLC, suggesting miR-137 as a potential therapeutic target for the treatment of NSCLC.  相似文献   

5.
目的探讨非小细胞肺癌(NSCLC)患者肺癌及癌旁组织中miR-10b(miR-10b)表达水平及miR-10b是否通过调控锌指转录蛋白基因(KLF4)对肺癌细胞系A549恶性化的影响。方法 40例NSCLC患者病理切片,原位杂交检测肺癌及癌旁组织中miR-10b的表达量;对肺癌细胞系A549转染miR-10b mimics后,CCK-8法检测肺癌细胞增殖;real-time PCR及Western blot检测KLF4 mRNA及蛋白水平;软琼脂克隆形成实验检测过表达miR-10b对A549细胞的肿瘤恶性化程度的影响。结果肺癌细胞A549及肺癌组织中miR-10b的表达量分别高于正常肺上皮细胞16HBE及癌旁组织;过表达miR-10b模拟物的A549细胞中,KLF4蛋白水平显著下降(P0.05);过表达的miR-10b可显著增加A549细胞的增殖速度及在软琼脂内的成瘤性。结论 miR-10b在不同类型细胞及组织中具有分布差异性、可能是通过抑制KLF4的表达促进肺癌细胞增殖及恶性化。  相似文献   

6.
目的探讨雷公藤甲素(TP)通过调控趋化因子受体4(CXCR4)基因表达对人非小细胞肺癌(A549)细胞增殖和凋亡的影响。方法实验分为4组:对照组、TP组(100 nm/L TP处理细胞)、CXCR4+TP组(转染质粒及TP处理细胞)和NC+TP组(转染空载质粒及TP处理细胞)。RT-qPCR和Western blot检测CXCR4表达以及转染效果;MTT法检测细胞增殖;AnnexinⅤ-FITC/PI双染色法检测细胞凋亡;Western blot检测增殖及凋亡相关蛋白表达。结果雷公藤甲素能够抑制A549细胞中CXCR4 mRNA和蛋白的表达(P<0. 05)。雷公藤甲素可抑制A549细胞增殖,诱导其凋亡(P<0. 05)。转染pc DNA-CXCR4能够上调CXCR4 mRNA和蛋白的表达(P<0. 05)。上调CXCR4的表达能够部分逆转雷公藤甲素对A549细胞增殖抑制和凋亡诱导的作用(P<0. 05)。结论雷公藤甲素可能通过下调CXCR4的表达抑制A549细胞增殖,诱导细胞凋亡。  相似文献   

7.
目的探讨circ-SFMBT2对非小细胞肺癌(non-small cell lung cancer,NSCLC)细胞生物学行为的影响以及对miR-7-5p/ADAM10分子轴的调控作用。方法﹑采用qRT-PCR法与Western印迹法分别检测NSCLC与癌旁组织中circ-SFMBT2、miR-7-5p、ADAM10的表达量;用Pearson法分析circ-SFMBT2与miR-7-5p,以及miR-7-5p与ADAM10的相关性;体外培养人支气管上皮样细胞(human bronchial epithelial-like cells,HBE)与肺癌细胞系H1650、H460、A549、H1299。用CCK-8与EdU实验检测细胞的增殖能力。用平板克隆形成实验检测细胞的克隆形成能力。用流式细胞术检测细胞凋亡率。用Transwell小室实验检测细胞侵袭。用双荧光素酶报告实验检测circ-SFMBT2与miR-7-5p、以及miR-7-5p与ADAM10的靶向关系。用裸鼠移植瘤实验检测敲低circ-SFMBT2对移植瘤生长的影响。用免疫组化实验检测移植瘤组织中ADAM10与Ki67蛋白阳性率。结果circ-SFMBT2与ADAM10在NSCLC组织及细胞系中表达升高,而miR-7-5p的表达降低,circ-SFMBT2与miR-7-5p的表达呈负相关,而miR-7-5p与ADAM10的表达呈负相关。沉默circ-SFMBT2及miR-7-5p过表达可抑制细胞增殖、克隆形成及侵袭,还可促进其凋亡。circ-SFMBT2可靶向调控miR-7-5p,而ADAM10是miR-7-5p的靶基因。沉默circ-SFMBT2与抑制miR-7-5p联合作用,以及miR-7-5p过表达与ADAM10过表达联合作用均可促进细胞增殖、克隆形成及侵袭,并抑制其凋亡。沉默circ-SFMBT2可抑制移植瘤的生长。结论︰沉默circ-SFMBT2可通过调控miR-7-5p/ADAM10分子轴而减弱NSCLC细胞增殖、克隆形成,侵袭能力并诱导其凋亡。  相似文献   

8.
目的探讨RNA干扰靶向抑制TEM8基因的表达对人非小细胞肺癌(non-small cell lung cancer,NSCLC)A549细胞增殖和侵袭能力的的影响。方法采用RT-PCR检测TEM8在5对NSCLC与癌旁正常组织中的表达;采用化学合成针对TEM8基因的小干扰RNA(TEM8 siRNA)下调A549细胞中该基因的表达,应用RT-PCR和Western blot法检测转染后细胞内TEM8的表达,通过Transwell侵袭实验检测TEM8对A549细胞侵袭能力的影响;CCK8实验及平板克隆形成实验检测TEM8对A549细胞增殖能力的影响。结果与癌旁正常肺组织相比,TEM8在NSCLC组织中显著高表达(P0.05),转染TEM8特异性siRNA后,A549细胞的增殖和侵袭能力均受显著抑制。结论 TEM8在NSCLC中呈过表达,干扰TEM8表达可明显抑制NSCLC的增殖与侵袭能力,推测TEM8可能成为治疗NSCLC的新靶点。  相似文献   

9.
目的:探讨circ-SFMBT2对非小细胞肺癌(non-small cell lung cancer,NSCLC)细胞生物学行为的影响以及对miR-7-5p/ADAM10分子轴的调控作用。方法:采用qRT-PCR法与Western印迹法分别检测NSCLC与癌旁组织中circ-SFMBT2、miR-7-5p、ADAM10...  相似文献   

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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.  相似文献   

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15.
Accumulating evidence has supported the concept that long noncoding RNAs (lncRNAs) participate in the initiation and progression of human cervical cancer (CC). The long intergenic nonprotein-coding RNA 173 (LINC00173) is a recently identified cancer-associated factor. However, the expression and biological role of LINC00173 in CC are poorly understood. Here, for the first time, we found that the expression of LINC00173 was decreased in CC tissues compared with that in nontumor tissues. Data from The Cancer Genome Atlas (TCGA) further revealed that the downregulated expression of LINC00173 in CC tissues was correlated with poor survival. Functionally, LINC00173 overexpression suppressed HeLa cell proliferation via induction of G0/G1 phase arrest. Ectopic expression of LINC00173 also repressed the invasiveness of HeLa cells. Conversely, LINC00173 depletion resulted in the enhanced proliferation and invasiveness of C33A cells. Mechanistically, LINC00173 functioned as a molecular sponge for miR-182-5p and inversely regulated the miR-182-5p level in CC cells. F-box and WD repeat domain-containing 7 (FBXW7) was identified as the target of miR-182-5p. LINC00173 overexpression enhanced the FBXW7 level via regulation of miR-182-5p in HeLa Cells. More importantly, the inhibitory effects of LINC00173 on HeLa cell proliferation and invasiveness were reversed by FBXW7 silencing. Taken together, the results indicate that the LINC00173/miR-182-5p/FBXW7 axis is critical for CC progression, which might offer new insights into effective therapy for CC.  相似文献   

16.

Objective

Non-small cell lung cancer (NSCLC) accounts for 80–85% of lung cancer cases which cause most of cancer-related deaths globally. As our previous study discovered miR-1260b can be regarded as a specific signature for metastasis in NSCLC patients. However, the molecular mechanisms of miR-1260b underlying NSCLC progression and metastasis remain dismal.

Methods

The expression of miR-1260b in NSCLC tissues and cell lines were examined by real-time PCR, the effects of miR-1260b on cell migration, invasion and proliferation were evaluated in vitro. Furthermore, luciferase reporter assay was performed to identify the targets of miR-1260b, and the association between miR-1260b and its target gene was determined by real-time PCR and western blot assay.

Results

The results showed that miR-1260b was significantly upregulated in NSCLC cell lines. The inhibition of miR-1260b expression decreased the migratory and invasive rates in A549 cells while miR-1260b overexpression had the opposite effect. Furthermore, PTPRK was identified as a direct target of miR-1260b, and PTPRK expression was inversely correlated with miR-1260b in NSCLC cell lines and clinical tissues.

Conclusions

These results suggested that miR-1260b may play an important role in NSCLC metastasis progression and could serve as a putative target for diagnosis and treatment of NSCLC.  相似文献   

17.
Background: Lung cancer is becoming the leading cause of cancer-related deaths with high mortality worldwide and in China as well. Non-small-cell lung cancer (NSCLC) is the most common type of lung cancer accounting for approximately 85% of all cases. Over 70% of cases are at loco-regionally advanced stages or have distant metastasis at the time of presentation with subsequently poor prognosis. MiRNAs are stable molecules in blood and used as biomarkers for the early diagnosis of various malignancy. The purpose of this study was to evaluate whether circulating miR-125a-5p, miR-145 and miR-146a could be used as biomarkers for the diagnosis of NSCLC through measuring their expression and assess their relationship with clinical pathological factors. Methods: Expression levels of serum miR-125a-5p, miR-145 and miR-146a were detected in 70 pairs of NSCLC patients and healthy controls using quantitative real-time PCR analysis. Results: Serum miR-125a-5p, miR-145 and miR-146a were overexpressed in NSCLC patients compared with healthy controls. Their values of the area under the receiver –operating characteristic curve (AUC-ROC) were 0.71, 0.84 and 0.78. Optimal sensitivity and specificity were 73.53% and 55.71%, 92.75% and 61.43%, 84.06% and 58.57%, respectively in differentiating NSCLC patients from healthy controls. Conclusions: These preliminary data suggest that serum miR-125a-5p, miR-145 and miR-146a may be useful noninvasive biomarkers for the clinical diagnosis of NSCLC.  相似文献   

18.
B7-H3 belongs to the co-inhibitory B7 family and plays an important role in the adaptive immune response in regulating T cells. In human malignancies, B7-H3 is reported to be involved in tumor immune evasion. However, the detailed molecular mechanism of B7-H3 in tumor evasion remains unclear, particularly in non-small cell lung cancer (NSCLC). Regulatory T cells (Tregs) are known as a key player in the inhibition of immune mechanisms. The study demonstrated the correlation between B7-H3 on tumor cells and the number of Tregs in the tumor microenvironment in NSCLC. B7-H3 was examined in tumor tissues from 110 patients with NSCLC by immunohistochemical analysis. Forkhead box P3+ (FOXP3+) Tregs in those spencimens were also detected and numbered. Survival curves were drawn using the Kaplan-Meier method and compared by the log-rank test. High B7-H3 expression in tumor cells significantly correlated with male gender, squamous NSCLC, advanced stage and shorter overall survival (OS) (P = 0.035, P = 0.004, P = 0.037, P = 0.014, respectively). Meanwhile, FOXP3 expression in tumor-infiltrating lymphocytes (TILs) was associated with male gender, regional lymph node involvement, advanced stage and worse OS (P = 0.009, P = 0.015, P = 0.014, P = 0.034, respectively). Significant correlation was identified between the expression of B7-H3 and the number of FOXP3+ TILs (P = 0.013). Patients with B7-H3 high/FOXP3 high had poorer OS (P = 0.006), suggesting that B7-H3 and Tregs may play a cooperatively role in tumor immune evasion, leading to poor outcomes for NSCLC patients.  相似文献   

19.
Background: A large number of studies demonstrated that microRNAs play important roles in the progression and development of human cancers. However, the expression level of miR-107 and its biological function in hepatocellular carcinoma (HCC) remains unclear. Method: Quantitative real-time PCR (qRT-PCR) was used to evaluate the expression level of miR-107 in HCC tissues and cell lines. Then, we explored the function of miR-107 to determine its potential roles on HCC cell proliferation in vitro. Luciferase reporter assay was used to confirm the target gene of miR-107, and the results were validated in cell lines. Results: miR-107 was significantly up-regulated in HCC tissues and cell lines. The enforced expression of miR-107 was able to promote cell proliferation in HepG2 cells. At the molecular level, our results suggested that expression of Axin2 was negatively regulated by miR-107. Conclusion: Our observations suggested that miR-107 could promote HCC cells proliferation via targeting Axin2 and might represent a potential therapeutic target for HCC.  相似文献   

20.
Recent evidence highlights that microRNAs serve as crucial regulators of tumorigenesis, including non-small cell lung cancer (NSCLC). The present study was designed to investigate the expression profile, clinical significance and biological role of miR-421 in NSCLC. The results showed that miR-421 expression was markedly increased in NSCLC tissues and cell lines. Further experimental data indicated that knockdown of miR-421 significantly inhibited NSCLC cell proliferation and induced cell cycle arrest in vitro. The migratory and invasive abilities of NSCLC cells were also attenuated following miR-421 knockdown. Furthermore, PDCD4 was identified as a direct target of miR-421, and its expression was inversely correlated with miR-421 expression in NSCLC tissues. PDCD4 also abrogated the oncogenic role of miR-421 in NSCLC cells. Collectively, our study revealed that miR-421 is significantly upregulated in NSCLC and might represent a potential therapeutic target for NSCLC patients.  相似文献   

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