c-MYC调节的miRNA-92b在结直肠癌发生发展中的功能及机制探究（英文）

micro RNAs(miRNAs)在参与癌症发生、发展过程中起着十分重要的作用.目前,miR-92b在结直肠癌中的作用及相关机制还未见报道.本研究探讨了miR-92b在结直肠癌发生发展中的功能及潜在机制.采用RT-qPCR方法发现,miR-92b在人结直肠癌临床样本中与癌旁组织相比显著高表达.通过结肠癌细胞株SW620稳转细胞及裸鼠皮下成瘤模型,发现过表达miR-92b可以显著促进细胞增殖及体内肿瘤生长.同时还发现miR-92b可以分泌形式存在于胞外及外周血中,提示miR-92b是一个具有分泌特性的micro RNA.在分子机理方面,c-MYC可通过调节miR-92b的启动子活性从而促进后者转录,并且c-MYC在结直肠癌组织样本中也存在高表达.进一步,通过在线预测、报告质粒活性检测及蛋白质印迹技术证实FBXW7是一个新的miR-92b靶基因.由于FBXW7已报道为c-MYC泛素降解过程中的关键泛素化连接酶之一,本研究结果提示结直肠癌中c-MYC、miR-92b及FBXW7三者间可能存在分子调节环路.综上所述,本研究为miR-92b在结直肠癌中的功能及机制提供了新的视角,并为miR-92b在结直肠癌早期诊断中的应用提供了新的参考.     

miR-598 对结直肠癌细胞转移潜能的影响

目的:探讨miR-598在结直肠癌转移中的作用和分子机制,为寻找新的结直肠癌治疗靶标提供理论依据。方法:收集30对人结直肠癌及癌旁正常组织标本,采用qRT-PCR检测miR-598的表达,采用Transwell和划痕实验确定miR-598对结直肠癌细胞侵袭和迁移能力的影响,利用在线靶基因预测软件,筛选出miR-598可能的下游靶基因Jagged 1(JAG1),利用Western blot及双荧光素酶报告基因实验检测miR-598对JAG1及上皮间质转化标志物(Vimentin及E-cadherin)表达的影响。结果:与正常肠黏膜组织对比,miR-598在结直肠癌组织中的表达水平明显降低;miR-598显著抑制结直肠癌细胞的侵袭及迁移能力;分子机制分析证实miR-598能够作用于JAG1的3'-UTR并抑制其表达;过表达miR-598显著下调Vimentin的表达水平,而提高E-cadherin的表达水平。结论:miR-598在人结直肠癌中表达明显下调;miR-598通过靶向调控靶基因JAG1的表达,抑制结直肠癌细胞EMT,从而有效的抑制了结直肠癌细胞的侵袭和迁移。     

MiR-26b是前列腺癌中的抑癌微RNA

microRNAs（又称miRNAs或miRs）是一类长度为19-24个核苷酸的单链非编码RNA分子。miRNA通过与其靶向的mRNA分子序列特异性互补配对,调节mRNA表达水平,抑制转录后的蛋白翻译。miRNA在肿瘤中既可作为致癌因子也可作为抑癌因。本研究前期已报道miR-26b在前列腺癌细胞系中低表达,并且抑制细胞自噬。本研究进一步全面揭示miR-26b对前列腺肿瘤细胞的作用。我们发现过表达miR-26b能够在体外抑制前列腺癌细胞的增殖和侵袭,并抑制裸鼠体内原位异种前列腺肿瘤的生长。为了探究miR-26b对前列腺癌细胞增殖和侵袭的潜在调控机制,我们进行了表达谱芯片鉴定miR-26b调控基因。表达谱芯片分析表明,在前列腺癌细胞系PC-3中过表达miR-26b后,显著上调的基因57个,显著下调的基因55个（变化倍数均大于2,且P值小于0.05）。差异基因的功能多与细胞增殖、凋亡调控、蛋白磷酸化和泛素化修饰调控过程相关,并且富集在多种信号通路中,例如TNF和TGF-β信号通路。在这些筛选出的基因中,CEACAM6表达水平下调2.17倍;序列分析及实验验证表明,CEACAM6的3’UTR区存在miR-26b的互补序列,是miR-26b的直接靶标。本研究证明了miR-26b能够靶向结合抑制CEACAM6的表达,从而抑制前列腺癌细胞在体外和体内的细胞增殖和侵袭活性,miR-26b是前列腺癌中的抑癌microRNA。     

MiR-26b是前列腺癌中的抑癌微RNA（英文）

微RNAs(又称miRNAs或miRs)是一类长度为19~24个核苷酸的单链非编码RNA分子.miRNA通过与其靶向的mRNA分子序列特异性互补配对,调节mRNA表达水平,抑制转录后的蛋白质翻译.miRNA在肿瘤中既可作为致癌因子也可作为抑癌因子.本研究前期已报道miR-26b在前列腺癌细胞系中低表达,并且抑制细胞自噬.本研究进一步全面揭示miR-26b对前列腺肿瘤细胞的作用.我们发现过表达miR-26b能够在体外抑制前列腺癌细胞的增殖和侵袭,并抑制裸鼠体内原位异种前列腺肿瘤的生长.为了探究miR-26b对前列腺癌细胞增殖和侵袭的潜在调控机制,我们进行了表达谱芯片鉴定miR-26b调控基因.表达谱芯片分析表明,在前列腺癌细胞系PC-3中过表达miR-26b后,显著上调的基因57个,显著下调的基因55个(变化倍数均大于2,且P值小于0.05).差异基因的功能多与细胞增殖、凋亡调控、蛋白质磷酸化和泛素化修饰调控过程相关,并且富集在多种信号通路中,例如TNF和TGF-β信号通路.在这些筛选出的基因中,CEACAM6表达水平下调2.17倍;序列分析及实验验证表明,CEACAM6的3′UTR区存在miR-26b的互补序列,是miR-26b的直接靶标.本研究证明了miR-26b能够靶向结合抑制CEACAM6的表达,从而抑制前列腺癌细胞在体外和体内的细胞增殖和侵袭活性,miR-26b是前列腺癌中的抑癌microRNA.     

塞内卡病毒通过激活自噬降解FBXW7拮抗宿主的抗病毒应答

【背景】塞内卡病毒(seneca valley virus, SVV)可引起猪严重的水疱性疾病,但目前仍无商业化疫苗,解析其与宿主抗病毒分子的相互作用具有重要意义。【目的】探究E3泛素连接酶(F-box and WD repeat domain containing 7, FBXW7)在抗SVV感染中的作用及其机制。【方法】利用小干扰技术敲低PK-15细胞FBXW7,结合RT-qPCR、组织半数感染量(tissue culture infective dose 50%,TCID50)和Western blotting分析FBXW7对SVV在PK-15细胞中复制及细胞因子的影响。【结果】Western blotting结果显示,SVV感染能够抑制PK-15细胞中FBXW7蛋白表达水平;敲低FBXW7后促进SVV复制,同时炎性细胞因子IL-6、IFN-β、TNF-αmRNA水平均显著降低;进一步研究显示,敲低ATG5抑制自噬后抑制FBXW7蛋白降解,SVV复制水平下降。【结论】本研究发现FBXW7对SVV复制具有抑制作用,SVV通过激活自噬介导FBXW7降解,为研发抗病毒靶点提供了新策略。     

miR-182靶向抑制FBXW7表达影响非小细胞肺癌细胞增殖研究

目的:研究microRNA-182(miR-182)在非小细胞肺癌(NSCLC)组织中的表达,并探讨其对NSCLC细胞增殖的影响及作用机制。方法:采用实时荧光定量PCR (qRT-PCR)检测miR-182在11例NSCLC及相应癌旁组织中的表达情况;Western blot检测FBXW7,c-Jun,c-Myc及cyclin D蛋白的表达;将miR-182模拟物,抑制物及相应空白对照瞬时转染H460细胞后,以细胞增殖与活性检测和克隆形成实验检测细胞系的增殖情况;流式细胞术检测细胞周期和凋亡变化;荧光素酶报告基因实验证实miR-182对FBXW7的靶向性作用。结果:NSCLC组织中miR-182的相对表达水平显著高于癌旁组织(P0.05)。转染组与对照组相比,H460细胞生长、克隆形成能力显著增强,细胞周期进程加快,细胞凋亡受到抑制(P0.05)。在NSCLC组织中,FBXW7蛋白的表达水平明显低于癌旁组织(P0.05)。miR-182 mimics显著降低野生型FBXW7质粒荧光素酶的活性,然而将结合位点突变后,miR-182 mimics则不再影响荧光素酶的活性。结论:miR-182在NSCLC组织中高表达,与FBXW7之间存在靶向关系,通过下调FBXW7蛋白表达促进NSCLC细胞的增殖,参与肿瘤的发生发展,预示其可能成为一种潜在的生物标志和治疗靶点。     

心肌细胞过表达miR-27b导致小鼠发生心肌纤维化和线粒体损伤

以往的miRNA芯片研究结果显示, miR-27b在人类心脏疾病标本和压力负荷引起的小鼠心肌肥厚模型中表达水平明显升高, 提示其在心脏疾病发生过程中发挥了重要功能。为研究miR-27b在心脏组织中的功能, 文章建立了在心肌细胞特异性 a-肌球蛋白重链(a-MHC)启动子(5.5 kb)控制下过表达miR-27b的转基因小鼠。通过Real-time PCR检测, 发现miR-27b前体和成熟体表达水平在转基因小鼠心脏组织中明显升高。miR-27b转基因小鼠不仅出现心肌肥厚, 还表现出明显的心肌纤维化。进一步研究表明心肌纤维化的关键调节分子金属基质蛋白酶13(MMP13)是miR-27b的靶分子, 在miR-27b转基因小鼠中MMP13显著下调, 胶原分子I和 III则显著上调。此外, 还发现miR-27b转基因小鼠会出现心脏超微结构的损伤。以上研究结果表明, miR-27b可能通过抑制MMP13促进心肌纤维化。     

心肌细胞过表达miR-27b导致小鼠发生心肌纤维化和线粒体损伤

以往的miRNA芯片研究结果显示, miR-27b在人类心脏疾病标本和压力负荷引起的小鼠心肌肥厚模型中表达水平明显升高, 提示其在心脏疾病发生过程中发挥了重要功能。为研究miR-27b在心脏组织中的功能, 文章建立了在心肌细胞特异性 a-肌球蛋白重链(a-MHC)启动子(5.5 kb)控制下过表达miR-27b的转基因小鼠。通过Real-time PCR检测, 发现miR-27b前体和成熟体表达水平在转基因小鼠心脏组织中明显升高。miR-27b转基因小鼠不仅出现心肌肥厚, 还表现出明显的心肌纤维化。进一步研究表明心肌纤维化的关键调节分子金属基质蛋白酶13(MMP13)是miR-27b的靶分子, 在miR-27b转基因小鼠中MMP13显著下调, 胶原分子I和 III则显著上调。此外, 还发现miR-27b转基因小鼠会出现心脏超微结构的损伤。以上研究结果表明, miR-27b可能通过抑制MMP13促进心肌纤维化。     

miR-190的表达下调有利于抑制结直肠癌

研究miR-190在结直肠癌(colorectal cancer,CC)患者中的表达和作用机制。采用Real-time PCR和探针原位杂交的方法检测miR-190在结直肠癌患者的癌组织和癌旁正常组织中的表达量变化。利用Targetscan数据库,寻找潜在的miR-190靶基因,并采用双荧光素酶报告基因验证。结果发现,相比于癌旁正常组织,miR-190在结直肠癌患者的癌组织中表达量显著下降(p0.000 1)。通过Targetscan数据库找到miR-190可作用于细胞因子IGF-1,双荧光素酶报告基因实验也证实了miR-190可以作用于IGF-1的3'UTR区域,从而抑制IGF-1的表达。在结直肠癌的发病过程中,miR-190表达量下降,导致IGF-1含量上升,进而促进了结肠癌的发展,miR-190具有抑癌作用。     

泛素连接酶FBW7的肿瘤抑制作用和机制

泛素-蛋白酶体系统是一个主要的蛋白质降解调节通路,在细胞分裂过程中发挥着重要作用,其成员在肿瘤中频繁存在着表达异常现象.FBW7又名AGO、hCDC4、FBXW7和SEL-10,是一种拥有7串联WD40重复结构域的F-box蛋白,可作为SCF型泛素连接酶（E3）复合物的底物识别亚基发挥作用.FBW7是一种肿瘤抑制蛋白,其基因在多种肿瘤包括直肠癌、胃癌、卵巢癌和白血病中存在着基因突变或缺失.FBW7可直接结合和靶向作用多种转录激活因子或原癌基因,如周期蛋白E、c-Myc、c-Jun、Notch、MCL1、KLF5 和mTOR等并对其进行泛素化修饰和随后的26S蛋白酶体降解.肿瘤抑制蛋白FBW7的研究对肿瘤发生机制的理解具有重要意义,同时也为肿瘤的诊断和治疗提供了新的靶点.本文综述了FBW7的特征、肿瘤抑制作用及机制.     

miR-367 stimulates Wnt cascade activation through degrading FBXW7 in NSCLC stem cells

Lung carcinoma tops the categories of cancer related motility, and has been treated as the main threat to human health. The functions and related mechanism of FBXW7 controlled lung cancer stem cells' signatures is barely unknown, and the miR-367 regulations of FBXW7 via Wnt signaling have not been explored. Cancer stem cells of either ALDH1+ or CD133+ phenotype were found to be referred to advanced stages in patients with NSCLC (non-small cell lung carcinoma). To study the roles of miR-367, we found greater miR-367 level or FBXW7 level was reserved in NSCLC than that of paired adjacent normal tissues, and their upregulations were positively correlated with Wnt signaling activation. On the contrary, increased miR-367 was correlated with Let-7 repression. MiR-367 was related to stronger sphere forming ability in stem cells of NSCLC. We then explored the functions of the endogenous miR-367 in stem-like cells isolated from NSCLC cell lines. In HEK-293 cells, we identified FBXW7 as the direct downstream gene of miR-367, which consequently released the LIN-28 dependent inhibition of suppressive Let-7. Through informatics analysis, miR-367 was predicated to function through Wnt signaling, and decreased Let-7 played the pivotal role to maintain TCF-4/Wnt pathway activity. The reintroduction of FBXW7 abolished the oncogenic stimulation of miR-367 on TCF-4 activity, with Wnt signaling factors depression. In conclusion, our findings demonstrated the oncogenic roles of miR-367 exerting on the self-renewal ability of cancer stem-like cells through degrading the suppressive FBXW7, eventually helping to maintain Wnt signaling activation through a LIN28B/Let-7 dependent manner.     

miR-30b,Down-Regulated in Gastric Cancer,Promotes Apoptosis and Suppresses Tumor Growth by Targeting Plasminogen Activator Inhibitor-1

Background

Gastric cancer is one of the most common malignant diseases worldwide. Emerging evidence has shown that microRNAs (miRNAs) are associated with tumor development and progression. Our previous studies have revealed that H. pylori infection was able to induce the altered expression of miR-30b in gastric epithelial cells. However, little is known about the potential role of miR-30b in gastric cancer.

Methods

We analyzed the expression of miR-30b in gastric cancer cell lines and human gastric cancer tissues. We examined the effect of miR-30b mimics on the apoptosis of gastric cancer cells in vitro by flow cytometry (FCM) and caspase-3/7 activity assays. Nude mouse xenograft model was used to determine whether miR-30b is involved in tumorigenesis of gastric cancer. The target of miR-30b was identified by bioinformatics analysis, luciferase assay and Western blot. Finally, we performed the correlation analysis between miR-30b and its target expression in gastric cancer.

Results

miR-30b was significantly down-regulated in gastric cancer cells and human gastric cancer tissues. Enforced expression of miR-30b promoted the apoptosis of gastric cancer cells in vitro, and miR-30b could significantly inhibit tumorigenicity of gastric cancer by increasing the apoptosis proportion of cancer cells in vivo. Moreover, plasminogen activator inhibitor-1 (PAI-1) was identified as the potential target of miR-30b, and miR-30b level was inversely correlated with PAI-1 expression in gastric cancer. In addition, silencing of PAI-1 was able to phenocopy the effect of miR-30b overexpression on apoptosis regulation of cancer cells, and overexpression of PAI-1 could suppressed the effect of promoting cell apoptosis by miR-30b, indicating PAI-1 is potentially involved in miR-30b-induced apoptosis on cancer cells.

Conclusion

miR-30b may function as a novel tumor suppressor gene in gastric cancer by targeting PAI-1 and regulating the apoptosis of cancer cells. miR-30b could serve as a potential biomarker and therapeutic target against gastric cancer.     

MicroRNA-375 inhibits colorectal cancer growth by targeting PIK3CA

Colorectal cancer (CRC) is the second most common cause of death from cancer. MicroRNAs (miRNAs) represent a class of small non-coding RNAs that control gene expression by triggering RNA degradation or interfering with translation. Aberrant miRNA expression is involved in human disease including cancer. Herein, we showed that miR-375 was frequently down-regulated in human colorectal cancer cell lines and tissues when compared to normal human colon tissues. PIK3CA was identified as a potential miR-375 target by bioinformatics. Overexpression of miR-375 in SW480 and HCT15 cells reduced PIK3CA protein expression. Subsequently, using reporter constructs, we showed that the PIK3CA untranslated region (3′-UTR) carries the directly binding site of miR-375. Additionally, miR-375 suppressed CRC cell proliferation and colony formation and led to cell cycle arrest. Furthermore, miR-375 overexpression resulted in inhibition of phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway. SiRNA-mediated silencing of PIK3CA blocked the inhibitory effect of miR-375 on CRC cell growth. Lastly, we found overexpressed miR-375 effectively repressed tumor growth in xenograft animal experiments. Taken together, we propose that overexpression of miR-375 may provide a selective growth inhibition for CRC cells by targeting PI3K/Akt signaling pathway.     

Restoration of miR-1228* Expression Suppresses Epithelial-Mesenchymal Transition in Gastric Cancer

Dysregulated miRNAs play critical roles during carcinogenesis and cancer progression. In the present study, the function of miR-1228* in regulating cancer progression was investigated in gastric cancer. Decreased expression of miR-1228* was observed in human gastric cancer tissues comparing to normal tissues. Subsequently, the role of miR-1228* was evaluated in vivo using the tumor xenograft model. In this model, miR-1228* overexpression suppressed xenograft tumor formation. Furthermore, we demonstrated miR-1228* negatively regulated NF-κB activity in SGC-7901 gastric cancer cells and found that CK2A2 was a target of miR-1228*. Upregulation of miR-1228* decreased the expression of mesenchymal markers and increased the epithelial marker E-cadherin, suggesting its potential role in suppressing epithelial-mesenchymal transition. Collectively, these findings provide the first evidence that miR-1228* plays an important role in regulating gastric cancer growth and suggest that selective restoration of miR-1228* might be beneficial for gastric cancer therapy.     

Inhibition of miR-92b suppresses nonsmall cell lung cancer cells growth and motility by targeting RECK

microRNAs play critical roles in the progression and metastasis of nonsmall cell lung cancer (NSCLC). miR-92b acts as an oncogene in some malignancies; however, its role in NSCLC remains poorly understood. Here, we found that miR-92b was significantly increased in human NSCLC tissues and cell lines. Inhibition of miR-92b remarkably suppressed cell proliferation, migration, and invasion of NSCLC cells. Reversion-inducing-cysteine-rich protein with kazal motifs (RECK) was identified to be a target of miR-92b. Expression of miR-92b was negatively correlated with RECK in NSCLC tissues. Collectively, miR-92b might promote NSCLC cell growth and motility partially by inhibiting RECK.     

miRNA-27b Targets Vascular Endothelial Growth Factor C to Inhibit Tumor Progression and Angiogenesis in Colorectal Cancer

Colorectal cancer (CRC) is one of the most prevalent cancers globally and is one of the leading causes of cancer-related deaths due to therapy resistance and metastasis. Understanding the mechanism underlying colorectal carcinogenesis is essential for the diagnosis and treatment of CRC. microRNAs (miRNAs) can act as either oncogenes or tumor suppressors in many cancers. A tumor suppressor role for miR-27b has recently been reported in neuroblastoma, while no information about miR-27b in CRC is available. In this study, we demonstrated that miR-27b expression is decreased in most CRC tissues and determined that overexpression of miR-27b represses CRC cell proliferation, colony formation and tumor growth in vitro and in vivo. We identified vascular endothelial growth factor C (VEGFC) as a novel target gene of miR-27b and determined that miR-27b functioned as an inhibitor of tumor progression and angiogenesis through targeting VEGFC in CRC. We further determined that DNA hypermethylation of miR-27b CpG islands decreases miR-27b expression. In summary, an anti-tumor role for miR-27b and its novel target VEGFC in vivo could lead to tumor necrosis and provide a rationale for developing miR-27b as a therapeutic agent.     

miR-144 suppresses cell proliferation and migration in colorectal cancer by targeting NRAS

Colorectal cancer (CRC) is a type of malignant cancer that has become particularly prevalent worldwide. It is of crucial importance to CRC treatment that the underlying molecular mechanism of CRC progression is determined. The NRAS gene is an important small G protein that is involved in various biological processes, including cancers. NRAS is an oncogene in many neoplasms but its function and regulation in CRC have seldom been investigated. In this study, it was uncovered that the NRAS protein was significantly upregulated in CRC tissues. According to a bioinformatics prediction, we identified that miR-144 may target NRAS to suppress its expression. In vitro experiments indicated that miR-144 decreased NRAS expression in different CRC cell lines (SW480, LoVo, and Caco2). By inhibiting NRAS, miR-144 repress SW480 cell proliferation and migration. Moreover, miR-144 decelerated the growth of SW480 xenograft tumors in vivo by targeting NRAS. In summary, our results identified a novel miR-144-NRAS axis in CRC that could promote the research and treatment of CRC.     

miR-29b suppresses tumor growth and metastasis in colorectal cancer via downregulating Tiam1 expression and inhibiting epithelial–mesenchymal transition

Recently, the role of miR-29b in colorectal carcinoma (CRC) development appears to be controversial. Until now, the expression and function of miR-29b in CRC have not been clarified clearly. We showed that decreased expression of miR-29b usually occurred in CRC cell lines and tissue samples. Loss- and gain-of-function assays in vitro revealed suppressive effects of miR-29b on cell proliferation and migration. Endogenous overexpression of miR-29b was sufficient to suppress aggressive behavioral phenotypes in mice. Proteomic analysis showed that miR-29b involved in integrate several key biological processes. In addition, miR-29b mediated the inhibition of epithelial–mesenchymal transition (EMT) and the inactivation of mitogen-activated protein kinase and phosphatidylinositol-4,5-bisphosphate 3-kinase/AKT signal transduction pathway. Further studies found that T lymphoma invasion and metastasis 1 (Tiam1) was identified as a direct target of miR-29b. In contrast to the phenotypes induced by miR-29b restoration, Tiam1-induced cell proliferation and migration partly rescued miR-29b-mediated biological behaviors. Our results illustrated that miR-29b as a suppressor has a critical role in CRC progression, which suggests its potential role in the molecular therapy of patients with advanced CRC.Colorectal cancer (CRC) is the third most commonly diagnosed cancer and the third leading cause of cancer death. In China, the incidence of CRC is continually increasing despite advances in treatment and subsequent improvement in prognosis. Metastasis leads to most of the mortalities and has a critical role in the poor prognosis.^{1, 2} The underlying molecular mechanisms in CRC metastasis are still unclear. Hence, it is urgent to identify important molecules in cancer progression, which may be used to develop new diagnostic strategies and drugs targeting these markers.MicroRNAs (miRNAs) are a class of diverse, small, noncoding RNAs that are processed from precursors with a characteristic hairpin secondary structure.³ They usually function as critical gene regulators. In recent years, a large number of studies have confirmed that miRNAs have important roles in tumorigenesis and metastasis by targeting different mRNAs.⁴ To date, abnormal expression of several miRNAs, such as miR-21,⁵ miR-124,⁶ miR-625,⁷ miR-339-5p⁸ and miR-27b,⁹ has been identified in CRC and may contribute to the development and progression of CRC. In our recent study, miR-133a was identified as a tumor-suppressive miRNA in human CRC that acts by repressing LIM and SH3 protein 1, which has been previously identified as tumor metastasis-associated protein,¹⁰ provides additional evidence of a pivotal role for miRNAs in CRC tumorigenesis and progression.¹¹miR-29b belongs to the miR-29b family that comprises three members: miR-29a, -29b and -29c. Recently, several studies have showed that miR-29b was dysregulated and represses tumor progression in hepatocellular,¹² ovarian,¹³ prostate,¹⁴ breast¹⁵ and gastric¹⁶ cancer. In colorectal cancer, increased miR-29b was found in colon cancer cells following exposure to a Hexane extract of American Ginseng (HAG) and suppressed the migration of colon cancer cells.¹⁷ In the other study, increased miR-29b was observed in ulcerative colitis-related CRC compared with ulcerative colitis, suggesting its function as oncogene.¹⁸ Thus, the role of miR-29b in CRC development appears to be controversial. Until now, the expression and function of miR-29b in CRC have not been clarified clearly.In this study, we detected miR-29b expression in CRC cells and tissue samples. Gain- or loss-of-function assays were used to analyze the effect of miR-29b on cell behaviors. We performed xenograft mice models to investigate its therapeutic role in tumor genesis and metastasis in vivo. Finally, we also explored the molecular mechanisms underlying the function of miR-29b and its potential targets.