MicroRNA-449a/b抑制人结肠癌细胞内Fra-1的表达

MicroRNAs (miRNAs) 是一类长度约为22 nt的非编码的调控性小RNA,它们在诸多的生命活动中发挥重要作用,如参与调控细胞的增殖、分化、凋亡以及肿瘤的发生发展. MicroRNA-449a/b (miR 449a/b) 是脊椎动物中进化保守的miRNA,作为抑癌基因,参与了许多癌症的发生过程,但其在结肠癌中的作用尚不清楚. 本文利用实时荧光定量技术研究了miR-449a/b在结肠癌组织中的表达. 利用双荧光素酶报告基因检测系统及Western印迹鉴定miR-449a/b的靶基因. 应用MTS法和Transwell分别检测miR-449a/b对结肠癌细胞增殖和迁移的影响. 检测组蛋白乙酰化酶抑制剂曲古菌素A (trichostatin A, TSA) 对结肠癌细胞中miR-449a/b表达的影响. 研究结果表明：与正常结肠组织相比,miR-449a/b在结肠癌组织中低表达;miR 449a/b能够结合到FRA-1 mRNA 3′-非翻译区 (3′-untranslated region, 3′-UTR),从而抑制结肠癌细胞HCT116内源Fra 1的表达;外源转染miR-449a/b明显抑制结肠癌细胞HCT116的增殖和迁移;并且TSA处理能够诱导结肠癌细胞HCT116中miR-449a/b的表达. 以上结果提示: miR-449a/b可能通过抑制靶基因Fra-1的表达,进而抑制结肠癌细胞的增殖和迁移．     

MicroRNA-19a targets tissue factor to inhibit colon cancer cells migration and invasion

The over-expression of tissue factor (TF) and its roles in colon cancer progression have attracted much attention. However, the mechanisms regulating TF expression have not yet been shown in detail. In this study, we over-expressed miR-19a, miR20a and miR-106b in colon cancer cells, and evaluated their impact on TF expression and cellular function. We provide evidence demonstrating that miR-19a inhibited TF expression in vitro. Luciferase reporter assay confirmed that TF was a direct target of miR-19a because the miR-19a mediated repression of luciferase activity was abolished by mutation of the putative binding site. Moreover, miR-19a suppressed colon cancer cell migration and invasion. This effect was due to the indirect down-regulation of matrix metalloproteinase 9. Finally, we investigated the relevance of TF and miR-19a expression in a total of 48 paired colon cancer samples and revealed that miR-19a was inversely correlated with TF expression in stages I and II cases. Therefore, our results suggested that miR-19a was capable of suppressing TF expression in vitro and inhibiting cell migration and invasion. Although it was not the unique mechanism responsible for the expression of TF in vivo, miR-19a was inversely correlated with TF expression in early stage colon cancer patients.     

miR-29b regulates migration of human breast cancer cells

microRNAs (miRNAs) are short non-coding RNAs that regulate gene expression by targeting mRNAs, inhibiting the expression of the associated proteins. Although a role for aberrant miRNA expression in cancer has been postulated, the pathophysiologic role and relevance of aberrantly expressed miRNAs in tumor biology has not been established. We evaluated the expression pattern of miRNAs in human breast cancer cells by qPCR, finding out an up-regulated miRNA miR-29b and studying its biological effect by migration assay. We defined a target gene PTEN by bioinformatics approach and western blot. In breast cancer cell line MDA-MB-231 cell, which migrate faster than MCF-7, we observed that miR-29b was highly over-expressed. Inhibition of miR-29b in cultured cells increased the expression of the phosphatase and tensin homolog (PTEN) tumor suppressor, promoting apoptosis, decreasing migration, and decreasing invasion. In contrast, enhanced miR-29b expression by transfection with pre-miR-29b decreased the expression of PTEN and impaired apoptosis, increasing tumor cell migration and invasion. Moreover, PTEN was shown to be a direct target of miR-29b and was also shown to contribute to the miR-29b-mediated effects on cell invasion. Modulation of miR-29b altered the role of PTEN involved in cell migration and invasion. Aberrant expression of miR-29b, which modulates PTEN expression, can contribute to migration, invasion, and anti-apoptosis.     

miR-223在结肠癌组织中的表达及促进结肠癌细胞迁移侵袭的机制研究

目的:探讨微小RNA-223 (mi R-223)在结肠癌组织中的表达及对结肠癌HT-29细胞侵袭、迁移能力的影响及机制。方法:检测mi R-223在结肠癌组织与癌旁组织中的表达。通过脂质体转染法将mi R-223模拟物(mi R-223 mimics,mi R-223 mimics组)及microRNA无关序列(mi R-223 NC,NC组)转染入结肠癌HT-29细胞。采用Real-time PCR检测转染后细胞中mi R-223和TWIST的表达,Western blot检测TWIST的蛋白表达,Tranwell检测细胞的迁移与侵袭能力。双荧光素酶报告基因检测mi R-223对TWIST基因启动子活性的影响。采用Transwell迁移与侵袭实验检测mi R-223 mimic及Twist si RNA共转染后人结肠癌细胞系HT-29迁移与侵袭能力的变化。结果:与癌旁结肠组织比较,mi R-223在结肠癌组织中呈现明显高表达(P0.05);与空白对照组和mi R-223 NC组比较,转染mi R-223 mimics后的HT-29细胞中的mi R-223表达显著增加(P0.05)。与阴性对照组和空载转染组相比较,mi R-223 mimics转染组穿透的细胞数目明显增加(P0.05),且mi R-223 mimics转染组的细胞侵袭能力显著增强(P0.05)。与mi R-223 NC组和空白对照组比较,转染mi R-223 mimics的HT-29细胞的TWIST基因m RNA和蛋白表达均显著增加(P0.05)。双荧光素酶检验结果显示TWIST为mi R-223的下游靶基因。共转染TWIST si RNA和mi R-223 mimics的结肠癌HT-29细胞的迁移与侵袭能力较单独转染mi R-223 mimics的HT-29细胞显著减弱(P0.05)。结论:mi R-223可能通过上调下游靶基因TWIST水平促进结肠癌HT-29细胞的迁移与侵袭。     

LncRNA miR143HG suppresses bladder cancer development through inactivating Wnt/β-catenin pathway by modulating miR-1275/AXIN2 axis

Although increasing long noncoding RNAs (lncRNAs) have been identified by high-throughput sequencing, their functions in human cancer remain largely unknown. The function of lncRNA miR143HG has not been explored before. In the present study, we found that miR143HG expression was significantly downregulated in bladder cancer tissues (BCa) compared with normal tissues. We showed that miR143HG high expression was associated with a high survival rate in BCa patients. Gain-of-function assays demonstrated that miR143HG overexpression suppressed the proliferation, arrested cell cycle progression, and attenuated migration and invasion of BCa cells in vitro. In vivo assay illustrated that ectopic expression of miR143HG inhibited BCa growth in vivo. Mechanistically, miR143HG was identified to inhibit the level of miR-1275, whereas miR-1275 directly targeted AXIN2, a negative regulator of the Wnt/β-catenin pathway. Restoration of miR-1275 or knockdown of AXIN2 significantly rescued the proliferation, migration, and invasion abilities of BCa cells. In summary, our findings demonstrated that miR143HG/miR-1275/AXIN2 axis regulates BCa development by modulating the Wnt/β-catenin pathway.     

SOX-17 is involved in invasion and apoptosis of colorectal cancer cells through regulating miR-302b-3p expression

The prognosis of advanced colorectal cancer (CRC) is currently still very poor, which suggests that the biological mechanisms of CRC oncogenesis are not fully understood. This study was conducted to explore the regulatory effect of SOX-17 on the expression of microRNA (miR)-302b-3p, and the involvement of SOX-17 in the invasion and apoptosis of CRC cells. The expression of SOX-17 and miR-302a,b,c,d-3p in colorectal cancer and normal colon epithelial cell lines was measured by real-time polymerase chain reaction and/or western blot. The regulatory effects of SOX-17 on miR-302b-3p gene in HT29 and LoVo cells were tested using the ChiP assay. The biological activities of SOX-17 and miR-302b-3p were evaluated by invasion and apoptosis assay. Results showed that transfection of SOX-17 small interfering RNA (siSOX-17) significantly increased, whereas transfection of SOX-17 overexpression vector (oeSOX-17) significantly decreased, miR-302b expression in HT29 and LoVo cells. Cotransfection of oeSOX-17 and miR-302b-3p inhibitor (INmiR-302b) significantly blocked the effects of SOX-17 in HT29 and LoVo cells. ChIP experiments showed that SOX-17 bonded to the miR-302b-3p promoter in HT29 and LoVo cells. Transfection of oeSOX-17 and miR-302b-3p mimics (MImiR-302b) significantly decreased, whereas transfection of siSOX-17 and INmiR-302b significantly increased, the invasion of HT29 and LoVo cells. In contrast, transfection of oeSOX-17 and MImiR-302b significantly increased, while transfection of siSOX-17 and INmiR-302b significantly decreased, apoptosis in HT29 and LoVo cells. Cotransfection of oeSOX-17 and INmiR-302b significantly blocked the effects of oeSOX-17 on cell invasion and apoptosis in HT29 and LoVo cells. These results suggested that SOX-17 can bind to the promoter of miR-302b-3p gene to regulate its expression, while both SOX-17 and miR-302b regulate the invasion and apoptosis in colorectal cancer cells.     

miRNA-29c Suppresses Lung Cancer Cell Adhesion to Extracellular Matrix and Metastasis by Targeting Integrin β1 and Matrix Metalloproteinase2 (MMP2)

Our pilot study using miRNA arrays found that miRNA-29c (miR-29c) is differentially expressed in the paired low-metastatic lung cancer cell line 95C compared to the high-metastatic lung cancer cell line 95D. Bioinformatics analysis shows that integrin β1 and matrix metalloproteinase 2 (MMP2) could be important target genes of miR-29c. Therefore, we hypothesized that miR-29c suppresses lung cancer cell adhesion to extracellular matrix (ECM) and metastasis by targeting integrin β1 and MMP2. The gain-of-function studies that raised miR-29c expression in 95D cells by using its mimics showed reductions in cell proliferation, adhesion to ECM, invasion and migration. In contrasts, loss-of-function studies that reduced miR-29c by using its inhibitor in 95C cells promoted proliferation, adhesion to ECM, invasion and migration. Furthermore, the dual-luciferase reporter assay demonstrated that miR-29c inhibited the expression of the luciferase gene containing the 3′-UTRs of integrin β1 and MMP2 mRNA. Western blotting indicated that miR-29c downregulated the expression of integrin β1 and MMP2 at the protein level. Gelatin zymography analysis further confirmed that miR-29c decreased MMP2 enzyme activity. Nude mice with xenograft models of lung cancer cells confirmed that miR-29c inhibited lung cancer metastasis in vivo, including bone and liver metastasis. Taken together, our results demonstrate that miR-29c serves as a tumor metastasis suppressor, which suppresses lung cancer cell adhesion to ECM and metastasis by directly inhibiting integrin β1 and MMP2 expression and by further reducing MMP2 enzyme activity. The results show that miR-29c may be a novel therapeutic candidate target to slow lung cancer metastasis.     

Retracted: MicroRNA-204-3p represses colon cancer cells proliferation,migration, and invasion by targeting HMGA2

Colon cancer is a detrimental neoplasm of the digestive tract. MicroRNAs (miRNAs) as central regulators have been discovered in colon cancer. Nonetheless, the impact of miR-204-3p on colon cancer remains indistinct. The research attempted to uncover the impacts of miR-204-3p on colon cancer cells growth, migration, and invasion. miR-204-3p expression level in colon cancer tissues and diverse colon cancer cell lines were testified by the quantitative real-time polymerase chain reaction. Exploration of the impacts of miR-204-3p on cell growth, migration, invasion, and their associated factors through assessment of CCK-8, flow cytometry, Transwell, and western blot, respectively. High mobility group AT-hook 2 (HMGA2) expression was then detected in Caco-2 cells after miR-204-3p mimic and inhibitor transfection, additionally dual-luciferase activity was implemented to further uncover the correlation between HMGA2 and miR-204-3p. The impact of HMGA2 on Caco-2 cell growth, migration, and invasion was finally assessed. We found that repression of miR-204-3p was discovered in colon cancer tissues and HCT116, SW480, Caco-2, HT29 and SW620 cell lines. MiR-204-3p overexpression mitigated Coca-2 cell viability, facilitated apoptosis, simultaneously adjusted CyclinD1 and cleaved caspase-3 expression. Cell migration, invasion, and the associated factors were all suppressed by miR-204-3p overexpression. Reduction of HMGA2 was presented in Caco-2 cells with miR-204-3p mimic transfection, and HMGA2 was predicated to be a target gene of miR-204-3p. Besides, HMGA2 silence showed the inhibitory effect on Caco-2 cells growth, migration, and invasion. In conclusion, miR-204-3p repressed colon cancer cell growth, migration, and invasion through targeting HMGA2.     

Up-regulation of miR-200b in biliary atresia patients accelerates proliferation and migration of hepatic stallate cells by activating PI3K/Akt signaling

An increasing body of evidence suggests that miRNAs are involved in fibrotic process of several organs including heart, lung and kidney. It has been observed recently that aberrant expression of miR-200s are associated with hepatic fibrosis. However, the role and underlying mechanism of miR-200s in hepatic fibrogenesis remains unknown. Here, we investigate the role of miR-200b in the activation of immortalized human hepatic stallate cells (HSCs), LX-2 cells. We firstly found that miR-200b significantly enhanced proliferation and migration of LX-2 cells. Secondly, our findings showed that miR-200b enhanced the phosphorylation of Akt, a downstream effector of phosphatidyl-inositol 3-Kinase (PI3K). FOG2, as the targets of fly miR-8 and human miR-200s, directly binds to p85α and inhibits the activation of the PI3K/Akt pathway. Here, we showed that FOG2 protein levels in LX-2 cells were suppressed significantly by miR-200b mimics. FOG2 knockdown by siRNAs activated the PI3K/Akt signaling, which increased cell growth and migration that mimicked the effect of miR-200b. Conversely, LY294002, a highly selective inhibitor of PI3K, could block phosphorylation of Akt and effect of miR-200b. In addition, we showed that miR-200b enhanced the expression of matrix metalloproteinase-2 (MMP-2), which may increase the migration of LX-2 cells. Finally, our results indicated that the expression of miR-200b was unregulated in the biliary atresia (BA) and associated with liver fibrotic progression. These data suggest a potential mechanism for Akt activation through FOG2 down-regulation by miR-200b that can lead to HSC growth and migration. In view of the putative pathogenic role of miR-200b in HSCs, miR-200b may constitute a potential marker for HSC activation and liver fibrosis progression.     

A positive feedback loop between miR‐181b and STAT3 that affects Warburg effect in colon cancer via regulating PIAS3 expression

This study aimed to investigate the relationship between the expression of microRNA (miR)‐181b, protein inhibitor of activated STAT3 (PIAS3) and STAT3, and to examine the function of the miR‐181b/PIAS3/STAT3 axis on the Warburg effect and xenograft tumour growth of colon cancer. Moreover, a positive feedback loop between miR‐181b and STAT3 that regulated the Warburg effect in colon cancer was explored. A luciferase reporter assay was used to identify whether PIAS3 was a direct target of miR‐181b. The gain‐of‐function and loss‐of‐function experiments were performed on HCT 116 cells to investigate the effect of miR‐181b/PIAS3/STAT3 on the Warburg effect and xenograft tumour growth of colon cancer, as determined by commercial kits and xenograft experiments. The relationship between the expression of miR‐181b, PIAS3 and STAT3 in HCT 116 and HT‐29 cells was determined using RT‐qPCR and Western blot. We found miR‐181b was a direct regulator of PIAS3. miR‐181b promoted the Warburg effect and the growth of colon cancer xenografts; however, these effects could be reversed by PIAS3. miR‐181b expression interacted with STAT3 phosphorylation in a positive feedback loop in colon cancer cells via regulating PIAS3 expression. In conclusion, this study for the first time demonstrated that miR‐181b contributed to the Warburg effect and xenograft tumour growth of colon cancer by targeting PIAS3. Moreover, a positive feedback loop between miR‐181b and STAT3 that regulated the Warburg effect in colon cancer was also demonstrated. This study suggested miR‐181b/PIAS3/STAT3 axis as a novel target for colon cancer treatment.     

The regulatory roles of miRNA and methylation on oncogene and tumor suppressor gene expression in pancreatic cancer cells

Carcinogenesis is driven by an accumulation of mutations and genetic lesions, which leads to activation of oncogenes and inactivation of tumor suppressor genes. However, the molecular mechanisms by which the expression of these genes was regulated in pancreatic cancer remains unclear. In this study, we investigated the regulatory effects of microRNA and methylation on the expression of k-ras, TP53 and PTEN genes in pancreatic cancer cells. The protein and miRNA levels were measured by Western blotting and Northern blotting, respectively. Xenograft pancreatic tumor models were established by inoculating BxPC-1, Capan-2, and Panc-1 tumor cells into athymic nu/nu mice. A disparate level of KRAS, p53, PTEN, Dnmts, and Dicer 1 proteins as well as let-7i, miR-22, miR-143, and miR-29b miRNA was observed in BxPC-1, Capan-2, and Panc-1 cells. Knockdown of Dicer 1 expression in BxPC-3 and Panc-1 cells resulted in significant increases in KRAS, p53, PTEN, and Dnmts protein levels and significant decreases in miR-22, miR-143, let-7i, and miR-29b expression. Knockdown of Dicer 1 expression in Capan-2 cells significantly increased p53 and PTEN expression, while significantly decreased miR-22 and miR-143 expression, but had no effects on PTEN, Dnmts, let-7i, and miR-29b expression. Knockdown of Dicer 1 expression significantly inhibited xenograft BxPC-3 tumor growth, but promoted xenograft Panc-1 tumor growth. In contrast, knockdown of Dicer 1 expression had no effect on xenograft Capan-2 tumor growth. Our study suggested that different pancreatic cancer cell lines exhibited obvious discrepancies in gene expression profiles, implying that different molecular mechanisms are involved in the carcinogenesis of pancreatic cancer subclasses. Our study highlighted the importance of personalized therapy.     

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.     

miR-125b targets ARID3B in breast cancer cells

Mounting evidence suggests involvement of deregulated microRNA (miRNA) expression during the complex events of tumorigenesis. Among such deregulated miRNAs in cancer, miR-125b expression is reported to be consistently low in breast cancers. In this study, we screened a panel of breast cancer cell lines (BCCLs) for miR-125b expression and detected decreased expression in 14 of 19 BCCLs. Due to the heterogeneity of breast cancers, MCF7 cells were chosen as a model system for ERBB2 independent breast cancers to restore miR-125b expression (MCF7-125b) to investigate the phenotypical and related functional changes. Earlier, miR-125b was shown to regulate cell motility by targeting ERBB2 in ERBB2 overexpressing breast cancer cells. Here we showed decreased motility and migration in miR-125b expressing MCF7 cells, independent of ERBB2. MCF7-125b cells demonstrated profoundly decreased cytoplasmic protrusions detected by phalloidin staining of filamentous actin along with decreased motility and migration behaviors detected by in vitro wound closure and transwell migration assays compared to empty vector transfected cells (MCF7-EV). Among possible numerous targets of miR-125b, we showed ARID3B (AT-rich interactive domain 3B) to be a novel target with roles in cell motility in breast cancer cells. When ARID3B was transiently silenced, the decreased cell migration was also observed. In light of these findings, miR-125b continues to emerge as an interesting regulator of cancer related phenotypes.     

Syndecan-2 Functions as a Docking Receptor for Pro-matrix Metalloproteinase-7 in Human Colon Cancer Cells

Although elevated syndecan-2 expression is known to be crucial for the tumorigenic activity in colon carcinoma cells, how syndecan-2 regulates colon cancer is unclear. In human colon adenocarcinoma tissue samples, we found that both mRNA and protein expression of syndecan-2 were increased, compared with the neighboring normal epithelium, suggesting that syndecan-2 plays functional roles in human colon cancer cells. Consistent with this notion, syndecan-2-overexpressing HT-29 colon adenocarcinoma cells showed enhanced migration/invasion, anchorage-independent growth, and primary tumor formation in nude mice, paralleling their morphological changes into highly tumorigenic cells. In addition, our experiments revealed that syndecan-2 enhanced both expression and secretion of matrix metalloproteinase-7 (MMP-7), directly interacted with pro-MMP-7, and potentiated the enzymatic activity of pro-MMP-7 by activating its processing into the active MMP-7. Collectively, these data strongly suggest that syndecan-2 functions as a docking receptor for pro-MMP-7 in colon cancer cells.     

Downregulation of microRNA-92b-3p suppresses proliferation,migration, and invasion of gastric cancer SGC-7901 cells by targeting Homeobox D10

To investigate the effect and mechanism of microRNA-92b-3p (miR-92b-3p) targeting Homeobox D10 (HOXD10) on proliferation, migration, and invasion of gastric cancer, we detected t he expression of miR-92b-3p and HOXD10 in SGC-7901 cells. The effects of miR-92b-3p or HOXD10 on proliferation, migration, invasion, and matrix metalloproteinase (MMP)-2/9 expression in SGC-7901 cells were measured by the Cell Counting Kit-8 assay, Transwell assay, and Western blot, respectively. The results showed that miR-92b-3p expression was increased, and HOXD10 expression was decreased in SGC-7901 cells, compared with human normal gastric epithelial cells GES-1. Functional experiments demonstrated that cell proliferation, migration, invasion, and expression of MMP-2/9 in SGC-7901 cells were significantly inhibited by miR-92b-3p silencing and HOXD10 overexpression. Moreover, HOXD10 was a potential target gene of miR-92b-3p as evidenced by the TargetScan software and double luciferase reporter assay. In the rescue experiment, knockdown of HOXD10, accompanied by higher expression of MMP-2/9, could significantly eliminate the inhibitory effects of miR-92b-3p silencing on cell proliferation, migration, and invasion. In conclusion, miR-92b-3p is highly expressed in gastric cancer SGC-7901 cells, and interfering with its expression might inhibit SGC-7901 cell proliferation, migration, and invasion via downregulating MMP-2/9 expression and targeting HOXD10.