• Cancers
• PAQR4
• Therapeutic target
• Tumor immunity
• miRNA

• Humans
• Neoplasms/genetics
• Neoplasms/drug therapy
• Neoplasms/pathology
• Drug Resistance, Neoplasm/genetics
• Oncogenes/genetics
• Molecular Targeted Therapy/methods
• Antineoplastic Agents/therapeutic use
• Membrane Proteins/genetics
• Animals
• Signal Transduction/genetics
• Signal Transduction/drug effects

• autophagy
• biomarker
• drug development
• uveal melanoma

• R35 ES030443 NIEHS NIH HHS

• Barrett’s esophagus
• epigenetics
• esophageal adenocarcinoma
• etiology
• gastroesophageal reflux disease
• genetics
• treatment

• ERC-StG 282079 and ERC-POC 632258 European Research Council

• breast cancer
• cell growth

Intervertebral disc degeneration (IVDD) is a prevalent cause of low back pain. IVDD is characterized by abnormal expression of extracellular matrix components such as collagen and aggrecan. In addition, it results in dysfunctional growth, senescence, and death of intervertebral cells. The biological pathways involved in the development and progression of IVDD are not fully understood. Therefore, a better understanding of the molecular mechanisms underlying IVDD could aid in the development of strategies for prevention and treatment. Autophagy is a cellular process that removes damaged proteins and dysfunctional organelles, and its dysfunction is linked to a variety of diseases, including IVDD and osteoarthritis. In this review, we describe recent research findings on the role of autophagy in IVDD pathogenesis and highlight autophagy-targeting molecules which can be exploited to treat IVDD. Many studies exhibit that autophagy protects against and postpones disc degeneration. Further research is needed to determine whether autophagy is required for cell integrity in intervertebral discs and to establish autophagy as a viable therapeutic target for IVDD.

• ECM degradation
• autophagy
• autophagy-targeting compounds
• intervertebral disc degeneration
• low back pain

• ARC
• FGF1
• circ_0122396
• miR-15a-5p

Esophageal cancer (ESCA) is a heterogeneous cancer with variable outcomes that are challenging to predict. MicroRNA (miR)-1269a is a newly discovered non-coding RNA that shows promising prognostic prediction in other cancers, but its clinical value in ESCA remains unclear.

To explore the relationship between miR-1269a and its clinical value and to develop a nomogram to succinctly display this relationship.

We analyzed the expression of miR-1269a in 125 ESCA tissue samples with complete clinical data and 52 normal tissue samples. We determined the prognostic value of miR-1269a for overall survival (OS) and cancer-specific survival (CSS) and evaluated the association between miR-1269a and clinical variables including tumor location, histologic grade, metastatic stage, and American Joint Committee on Cancer (AJCC) stage using multivariate Cox analysis. Additionally, we developed a nomogram for OS and CSS based on miR-1269a expression using age and AJCC stage and assessed its prognostic performance. Using Gene Ontology and Kyoto Encyclopedia of Gene and Genomes analyses, we predicted the target genes of miR-1269a and analyzed their potential function in caner development.

The expression of miR-1269a was significantly higher in ESCA patients than healthy controls. Patients with high expression of miR-1269a showed poor prognosis in OS and CSS, suffered increased rates of low differentiation and metastasis, and exhibited tumor stage T3 + T4, positive lymph stage, and AJCC stage III + IV. The area under the receiver operating characteristic curve of miR-1269a was 0.716 for OS and 0.764 for CSS. Multivariate Cox analysis revealed that AJCC stage and miR-1269a were independent factors for OS and CSS. Combing with age, we constructed a nomogram for prognostic prediction. Additionally, our nomogram showed excellent predictive performance for OS and CSS after 3 years and 5 years and was easy to use. Ultimately, the functional analysis suggested that miR-1269a was mostly involved in the PI3K-AKT signaling pathway.

miR-1269a can be used as a potential indicator for the prognosis of ESCA patients. We developed an easy-to-use nomogram with excellent ESCA prognostic prediction for clinical use.

• MicroRNA-1269a
• Esophageal cancer
• Prognosis
• Overall survival
• Cancer-specific survival

• diagnosis
• gallbladder neoplasms
• novel biomarker
• prognosis

Esophageal cancer is one of the most common cancers worldwide with poor prognosis and high mortality. The transcription factor SNAI1, encoding Snail1, is important for metastatic progression in esophageal cancer whereas the microRNA (miRNA)-203 has been shown to function as an inhibitor of metastasis in EC. The Snail1 protein is stabilized in EC partially by the deubiquitinating enzyme USP26; however, how USP26 is regulated is not completely known.

Expression of SNAI1 and USP26 messenger RNA (mRNA) and miR-203 was performed in datasets within The Cancer Genome Atlas and Gene Expression Omnibus, respectively. Expression of Snail1 and USP26 protein and miR-203 was determined in the normal esophageal cell line HET-1A and EC cell lines Kyse150 and TE-1 using western blot and quantitative polymerase chain reaction, respectively. TargetScan was used for in situ prediction of miR-203 targets and in vitro heterologous reporter assays using the wild-type and miR-203 seed mutant of the 3′ Untranslated region (UTR) of USP26 were used to investigate whether USP26 is a target of miR-203. Effects of increasing miR-203 using MIR203A/5P mimic on USP26 and Snail1 in the HET-1A, Kyse150 and TE-1 cell lines were performed using western blot and cycloheximide-based protein stability analysis. Effects of modulating miR-203 in Kyse150 and TE-1 cell lines on in vitro pro-metastatic effects were analyzed by invasion assay, scratch wound-healing assay, and chemosensitivity to 5-fluoruracil (5-FU). In vivo lung metastasis assay was used to study the effect of modulating miR-203 in Kyse150 cells.

SNAI1 mRNA and HSA/MIR203 was higher and lower, respectively, in EC patients compared to tumor-adjacent normal tissues. No changes in expression of USP26 mRNA were observed in these datasets. MIR/203 expression was downregulated whereas protein expression of both Snail1 and USP26 were higher in EC cell lines Kyse150 and TE-1 compared to normal esophageal cell line HET-1A. USP26 was predicted as a potential target of miR-203 by TargetScan Release 2.0. Reporter assays confirmed USP26 as a target of miR-203 in the EC cell lines. Transfection of EC cell lines with MIR203 mimic decreased USP26 protein expression and Snail1 protein stability indicating the ability of miR-203 to regulate Snail1 protein levels via USP26. Exogenous increase in miR-203 in the EC cell lines significantly inhibited Snail-1 mediated in vitro pro-metastatic function of invasion, wound-healing, and increased chemosensitivity to 5-FU. Finally, overexpression of miR-203 inhibited in vivo lung metastasis of Kyse150 cells, which was reversed following overexpression of USP26, indicating a direct role of miR-203-mediated regulation of USP26 in metastatic progression of EC.

Cumulatively, these results establish an important mechanism by which decrease in miR-203 expression potentiates metastatic progression in EC via USP26-mediated stabilization of Snail1. Hence, miR-203 can serve as a biomarker of metastasis in EC and is a potential target for therapeutic intervention in EC.

• Esophageal cancer
• Metastasis
• Snail1
• USP26
• miR-203

Long noncoding RNAs (lncRNAs) can promote hepatocellular carcinoma (HCC) initiation and progression. In this report, we examined the role of lncRNA LINC02476 in HCC.

The expression levels of different lncRNAs in HCC were explored using the TCGA database and lncRNA LINC02476 was selected for further study. The expression of LINC02476 in HCC tissues was determined by real-time PCR. The clinicopathological characteristics of HCC patients were analyzed relative to the expression of LINC02476. The expression of LINC02476 was downregulated in HCC cells using a lentiviral vector and different assays were performed to study cell growth, proliferation, invasion, apoptosis and the cell cycle. MiR-497 was selected as a miRNA that could interact with LINC02476 which was further tested by RNA immunoprecipitation. HMGA2 was selected as a possible target of miR-497, and their interaction was examined by a luciferase reporter assay.

LINC02476 expression was elevated in HCC cell lines and HCC tissues. When LINC02476 was downregulated, the growth and the invasion of HCC cells decreased in vitro and in vivo. LINC02476 negatively regulated the expression of miR-497 by acting as a ceRNA. HMGA2 was directly targeted and inhibited by miR-497.

The results indicate that LINC02476 functions through the miR-497/HMGA2 axis and that it has a role in the growth and metastasis of HCC cells. Therefore, LINC02476 could be an interesting new molecular target in HCC therapies.

• HMGA2
• LINC02476
• hepatocellular carcinoma
• miR-497

RIOK2 is a member of RIO (right open reading frame) kinase family. Recent studies have revealed the involvement of RIO kinases in glioma cell growth and expansion. However, the role and mechanism of RIOK2 in glioma cell migration and invasion remain unclear. Wound healing assay, Transwell assay and real‐time quantitative PCR (qRT‐PCR) detection of matrix metalloproteinases (MMPs) were used to evaluate the migration/invasion of glioma cells. Western blot and qRT‐PCR were employed to measure the expression of epithelial‐mesenchymal transition (EMT) markers. Dual luciferase reporter assay was performed to determine the binding between RIOK2 and miR‐4744. In addition, RIOK2 and miR‐4744 levels were quantified by qRT‐PCR and/or immunohistochemistry in glioma tissues. Transfection of RIOK2 siRNAs significantly inhibited glioma cell migration and invasion and down‐regulated the expression of MMPs (MMP2 and MMP9) and mesenchymal markers (N‐cadherin, β‐catenin, Twist1, fibronectin, ZEB‐1) in glioma cells. Overexpression of RIOK2 showed the opposite effects. MiR‐4744 directly bound to the 3'‐untranslated region of RIOK2 and negatively regulated the expression of RIOK2. Up‐regulation of miR‐4744 inhibited the migration and invasion of glioma cells. Overexpression of RIOK2 could reverse the effects of miR‐4744 up‐regulation on the migration, invasion and EMT process in glioma cells. Moreover, RIOK2 was high, while miR‐4744 was low in glioma tissues, and a negative correlation was found between them. These results suggest that RIOK2 is post‐transcriptionally targeted by miR‐4744, the low miR‐4744 and high RIOK2 levels in glioma may contribute to tumour cell infiltration through promoting the EMT.

• N-cadherin
• RIOK2
• fibronectin
• glioma
• miR-4744
• β-catenin

Endoscopic submucosal dissection (ESD) is an effective treatment of early esophageal adenocarcinomas (EACs). The decision of ESD over esophagectomy is based on clinical evaluation of tumor depth and invasion. On a molecular level, tumor invasion is strongly associated with epithelial-to-mesenchymal transition (EMT). Here, we investigated whether localized ESD-resected and surgically resected EAC samples displayed different expression profiles of EMT protein and microRNA markers and whether these different expression profiles were able to retrospectively discriminate localized and surgically resected samples. By doing this, we aimed to evaluate whether preoperative measurement of EMT marker expression might support the decision regarding ESD over surgery. The results showed that ESD-resected samples displayed an epithelial expression profile, i.e., high expression of epithelial protein markers, whereas surgically resected samples displayed high expression of mesenchymal markers. In addition, the anti-EMT microRNA-205 was significantly more expressed in ESD-resected samples, whereas we found no significant differences in the expression levels of microRNA-200 family members. Furthermore, in our retrospective approach, we have demonstrated that measurement of selected EMT markers and microRNA-205 has significant discrimination power to distinguish ESD-resected and surgically resected samples. We suggest that the assessment of EMT status of EAC samples on a molecular level may support clinical evaluation regarding the applicability of ESD.

• E-cadherin
• EMT
• ESD
• endoscopic submucosal dissection
• epithelial-to-mesenchymal transition
• esophageal adenocarcinoma
• microRNA-200 family
• microRNA-205

Increasing evidence has suggested that microRNAs (miRNAs) act as key post-transcriptional regulators in tumor progression. Previous studies have confirmed that miR-17-5p functions as an oncogene in multiple cancers and contributes to tumor progression. However, the role and biological functions of miR-17-5p in the development of laryngeal squamous cell carcinoma (LSCC) still remain unknown.

qRT-PCR was used to detect miRNA and mRNA expression levels in LSCC tissues and cell lines. CCK-8 assay was used to measure cell viability and flow cytometry was performed to evaluate cell apoptosis. Western blot analysis was used to detect the protein levels of BAX, BCL-2, cleaved Caspase-3, PIK3R1 and AKT. Luciferase reporter assay was used to detect the effect of miR-17-5p on PIK3R1 expression. Xenograft animal model was used to test the effect of miR-17-5p on LSCC cell in vivo.

In the present study, we found that miR-17-5p expression level was upregulated in LSCC tissues and cell lines. Depletion of miR-17-5p in LSCC cells significantly reduced cell proliferation and promoted cell apoptosis in vitro and in vivo. Mechanically, knockdown of miR-17-5p in LSCC cells inhibited BCL-2 expression while enhanced BAX and cleaved Caspase-3 protein expression. Moreover, depletion of miR-17-5p in LSCC cells suppressed AKT phosphorylation but did not influence PTEN expression. Importantly, miR-17-5p positively regulated PIK3R1 expression by directly binding to its 3′-untranslated region (UTR). Additionally, PIK3R1, which expression was downregulated in LSCC tissues and cell lines, was involved in LSCC cell survival by modulating the activation of AKT signal pathway. Dysregulation of miR-17-5p/PIK3R1 axis was participated in LSCC cell proliferation and apoptosis by inhibiting the activation of the PI3K/AKT signaling pathway.

In conclusion, our study indicates that the miR-17-5p/PIK3R1 axis plays an essential role in the development of LSCC and provides a potential therapeutic target for LSCC treatment.

• Apoptosis
• Laryngeal squamous cell carcinoma
• PIK3R1
• Proliferation
• miR-17-5p

We analyzed data from two non-coding RNA profiling arrays made available by the Gene Expression Omnibus (GEO) and found 17 miRNAs with remarkable differential expression between malignant and normal esophageal tissue. Correlation analysis between expression of these 17 miRNAs and patients’ clinicopathological characteristics showed that miR-203 was down-regulated in esophageal carcinoma (EC) tissues and was significantly associated with lymph node metastasis and poor overall survival. Overexpression of miR-203 significantly attenuated cellular proliferation, migration and invasion by EC cells in culture. Additionally, gene expression profiles and bioinformatics analysis revealed KIF5C to be a direct target of miR-203, and KIF5C overexpression partially counteracted the tumor inhibitory effects of miR-203 on EC cells. We also observed that miR-203, reduced KIFC5 protein levels, promoted cytoplasmic accumulation of Axin2, and reversed the invasive phenotype of EC cells. Taken together, these data demonstrate that miR-203 is a tumor suppressor in EC cells and its expression level could potentially be used as a prognostic indicator for EC patient outcomes.

• KIF5C
• esophageal carcinoma
• miR-203

In the past few years, exosomes released from adipose-derived stem cells (abbreviated as ADSCs) have shown promises to provide therapeutic benefits in the fields of regenerative medicine. miRNAs, existing in exosomes, are endogenous, small noncoding RNAs that play important roles in a variety of cellular functions and tumor development. Emerging evidences have indicated that miR-21 is one of the important miRNAs associated with tumor angiogenesis. In this study, we identified the role of exosomes from ADSCs overexpressing miR-21 in regulating/promoting vascularization of endothelial cells. Experimental data indicated an elevated miR-21 level in exosomes released by ADSCs overexpressing miR-21. In vitro matrigel angiogenesis assay showed that exosomes secreted by ADSCs overexpressing miR-21 significantly promoted the vascularization of HUVEC cells (an endothelial cell line). Quantitative real-time polymerase chain reaction (qRT-PCR) and western blot (WB) revealed an upregulation of HIF-1α, VEGF, SDF-1, p-Akt, p-ERK1/2 and downregulation of PTEN in response to miR-21 overexpression, indicating that miR-21 enriched exosomes induced angiogenesis through Akt and ERK activation and also HIF-1α and SDF-1 expression. Our work suggests that exosomes from ADSCs that overexpressing miR-21 can potentially promote vascularization and therefore the transplantation of exosomes from their culture may be suitable for clinical effort in regenerative medicine.

Background: Dysregulation of a single miRNA can play an essential role in tumor development and progression. Recent studies have shown that miR-382-5p can function as an oncogene or as a tumor suppressor in different types of cancers. However, the role of miR-382-5p in glioma growth and expansion has not been characterized.

Methods: Quantitative real time-PCR (qRT-PCR) was used to measure miR-382-5p levels in glioma tissues. The miR-382-5p mimics and inhibitors were employed to upregulate and downregulate miR-382-5p expression respectively in glioma cells. EdU assay was used to assess cell proliferation. Wound healing and Transwell assays were employed to evaluate cell migration and invasion. Western blot was used to measure the changes of epithelial-to-mesenchymal transition (EMT) markers and the potential miR-382-5p target genes.

Results: We found that miR-382-5p levels were low in glioma tissues as determined by qRT-PCR. EdU assay showed that upregulation of miR-382-5p significantly decreased cell proliferation in both U87 and U251 cells. Wound healing rate was significantly decreased in response to miR-382-5p mimics and significantly increased in response to miR-382-5p inhibitors. Transwell migration assays further confirmed the inhibitory effects of miR-382-5p on the migration in both U251 and U87 cells. Transwell invasion assays showed that upregulation of miR-382-5p resulted in a remarkable decrease in the number of invading cells, whereas downregulation of miR-382-5p led to a significant increase in the numbers of invading U87 and U251 cells. In addition, overexpression of miR-382-5p decreased the protein levels of N-cadherin, Snail and Slug, and increased E-cadherin levels, in glioma cells. Furthermore, miR-382-5p levels negatively correlated with Y box-binding protein 1 (YBX1) in lower grade glioma tissues, and negatively regulated the expression of YBX1 in glioma cells.

Conclusion: In summary, miR-382-5p inhibited proliferation, migration, invasion, and the EMT in glioma cells, possibly through targeting the oncogene YBX1.

• glioma
• invasion
• miR-382
• migration
• proliferation

• biomarker
• metastatic prostate cancer
• microRNA
• platinum drug resistance

• Esophageal squamous cell carcinoma
• LASP1
• cell progression
• miR-143

• LASSO regression model
• competitive endogenous RNA network
• diagnosis
• esophagus cancer

• HOXB1
• Metastasis
• NF-kB
• Osteosarcoma
• microRNAs

• FOXM1
• esophageal squamous cell carcinoma
• miR-34a

• Metastasis
• Osteosarcoma
• Proliferation
• SOX9
• miR-590-3p

• ABC transporters
• biomarker
• cancer
• chemotherapy
• esophagus
• prognosis
• radiotherapy

• ATP-Binding Cassette Transporters/genetics
• ATP-Binding Cassette Transporters/metabolism
• Biomarkers, Tumor/genetics
• Biomarkers, Tumor/metabolism
• Epigenesis, Genetic
• Esophageal Neoplasms/genetics
• Esophageal Neoplasms/metabolism
• Esophageal Neoplasms/therapy
• Humans
• Neoadjuvant Therapy/methods
• Polymorphism, Genetic

Ovarian cancer is among the leading cause of cancer-related deaths in females. In this study, we demonstrated that miR-595 expression was downregulated in the ovarian cancer tissues and cell lines. miR-595 expression was lower in the lymph node metastases tissues than in the primary ovarian cancer tissues and normal tissues. Furthermore, miR-595 overexpression suppressed the ovarian cancer cell proliferation, colony formation and invasion and promoted the sensitivity of ovarian cancer cell to cisplatin. We identified ABCB1 as a direct target gene of miR-595 in the ovarian cancer cell. ABCB1 expression was upregulated in the ovarian cancer tissues and cell lines. Morevoer, the expression level of ABCB1 was inversely correlated with miR-595 in the ovarian cancer tissues. In addition, overexpression of ABCB1 decreased the miR-595-overexpressing HO8910PM and SKOV-3 cell sensitivity to cisplatin. Ectopic expression of ABCB1 promoted the miR-595-overexpressing HO8910PM and SKOV-3 cell proliferation, colony formation and invasion. These data suggested that miR-595 acted a tumor suppressor role in ovarian cancer development and increased the sensitivity of ovarian cancer to cisplatin.

• ABCB1
• miR-595
• microRNAs
• ovarian cancer

• TGF-β
• glioblastoma
• microRNA-564
• proliferation

The incidence of gastro-esophageal disease and associated rate of esophageal adenocarcinoma (EAC) is rising at an exponential rate in the United States. However, research targeting EAC is lagging behind, and much research is needed in the field to identify ways to diagnose EAC early as well as to improve the rate of pathologic complete response (pCR) to systemic therapies. Esophagectomy with subsequent reconstruction is known to be a morbid procedure that significantly impacts a patient's quality of life. If indeed the pCR rate of patients can be improved and those patients destined to be pCR can be identified ahead of time, they may be able to avoid this life-altering procedure. While cancer-specific biological pathways have been thoroughly investigated in other solid malignancies, much remains unexplored in EAC. In this review, we will highlight some of the latest research in the field in regards with EAC, along with new therapeutic targets that are currently being explored. After reviewing conventional treatment and current changes in medical therapy for EAC, we will focus on unchartered grounds such as cancer stem cells, genetics and epigenetics, immunotherapy, and chemoradio-resistant pathways as we simultaneously propose some investigational possibilities that could be applicable to EAC.

• cancer stem cells
• chemoradioresistance
• esophageal adenocarcinoma
• genetic and epigenetic targets
• immunotherapy

• ROCK1
• glioblastoma
• miR-300
• microRNAs

• HDAC6
• HNSCC
• MiR-206
• PTEN/AKT/mTOR pathway
• Progression

Dysregulation of microRNAs (miRs) can contribute to cancer development and progression. In the present study, the function and underlying molecular mechanisms of miR-320 in breast cancer tumorigenesis and progression were investigated. The results of a reverse transcription-quantitative polymerase chain reaction analysis demonstrated that miR-320 was frequently downregulated in breast cancer tissues compared with adjacent normal tissues. In addition, knockdown of miR-320 in breast cancer cell lines promoted cell proliferation and invasion in vitro, whereas miR-320 overexpression had the opposite effect. Furthermore, a Dual-Luciferase reporter assay indicated that SRY-box 4 (SOX4) is a direct target of miR-320, and the restoration of SOX4 in miR-320-overexpressing cells attenuated the tumor-suppressive effects of miR-320. Collectively, these results indicated that miR-320 acts as a tumor suppressor in breast cancer tumorigenesis and progression.

• SRY-box 4
• breast cancer
• epithelial-mesenchymal transition
• microRNA 320

• Cataract
• miRNAs
• microRNAs

• Cisplatin
• carboplatin
• chemoresistance
• melanoma
• microRNA
• ovarian cancer

• Ovarian cancer
• TWIST1
• miR-320
• microRNAs

• PDK1
• miR-379
• microRNA
• osteosarcoma

• Adolescent
• Animals
• Base Sequence
• Cell Line, Tumor
• Cell Proliferation/genetics
• Child
• Disease Progression
• Down-Regulation/genetics
• Female
• Gene Expression Regulation, Neoplastic
• Humans
• Male
• Mice, Nude
• MicroRNAs/genetics
• MicroRNAs/metabolism
• Neoplasm Invasiveness
• Osteosarcoma/genetics
• Osteosarcoma/pathology
• Protein Serine-Threonine Kinases/genetics
• Protein Serine-Threonine Kinases/metabolism
• Pyruvate Dehydrogenase Acetyl-Transferring Kinase
• Up-Regulation/genetics
• Xenograft Model Antitumor Assays

• HOXC6
• chemosensitivity
• hepatocellular carcinoma
• miR-147
• migration
• proliferation

• Osteosarcoma
• Rab23
• miR-665
• microRNAs

• Cancer in vitro growth
• Cancer in vivo growth, FMNL3
• Esophageal squamous cell carcinoma
• MiR-127

• Laryngeal squamous cell carcinoma
• ROS1
• miR-300
• miRNAs
• microRNAs

• epidermal growth factor receptor
• microRNA-143
• non-small cell lung cancer

• Hes1
• MicroRNAs
• Neural stem cells
• differentiation
• miR-765

• Esophageal cancer
• MicroRNA
• Treatment

Gastric cancer (GC) is one of the most common malignant tumors worldwide. Emerging evidence has shown that abnormal microRNAs (miRNAs) expression is involved in tumorigenesis. MiR-329 was previously reported to act as a tumor suppressor or oncogene in some types of cancer. However, its function in gastric cancer (GC) is unclear. Here, we found that miR-329 was down-regulated in GC compared with adjacent controls. Enforced expression of miR-329 inhibited proliferation, migration and invasion of gastric cancer cells in vitro. We identified T lymphoma invasion and metastasis 1 (TIAM1) gene as potential target of miR-329. MiR-329 levels inversely correlated with TIAM1 expression in GC. Importantly, TIAM1 rescued the miR-329-mediated inhibition of cell invasion and proliferation. Finally, reintroduction of miR-329 significantly inhibited tumor formation of GC in the xenograft mice. Our findings suggest that miR-329 is a tumor suppressor and potential therapeutic target of GC

• TIAM1
• gastric cancer
• miR-329
• microRNAs

• Esophageal squamous carcinoma
• TRAF5
• miR-26a
• miR-26b
• migration
• proliferation