Turning sublimed sulfur and bFGF into a nanocomposite to accelerate wound healing via co-activate FGFR and Hippo signaling pathway.

Clinical treatment of diabetic refractory ulcers is impeded by chronic inflammation and cell dysfunction associated with wound healing. The significant clinical application of bFGF in wound healing is limited by its instability in vivo. Sulfur has been applied for the treatment of skin diseases in the clinic for antibiosis. We previously found that sulfur incorporation improves the ability of selenium nanoparticles to accelerate wound healing, yet the toxicity of selenium still poses a risk for its clinical application. To obtain materials with high pro-regeneration activity and low toxicity, we explored the mechanism by which selenium-sulfur nanoparticles aid in wound healing via RNA-Seq and designed a nanoparticle called Nano-S@bFGF, which was constructed from sulfur and bFGF. As expected, Nano-S@bFGF not only regenerated zebrafish tail fins and promoted skin wound healing but also promoted skin repair in diabetic mice with a profitable safety profile. Mechanistically, Nano-S@bFGF successfully coactivated the FGFR and Hippo signalling pathways to regulate wound healing. Briefly, the Nano-S@bFGF reported here provides an efficient and feasible method for the synthesis of bioactive nanosulfur and bFGF. In the long term, our results reinvigorated efforts to discover more peculiar unique biofunctions of sulfur and bFGF in a great variety of human diseases.

Acesulfame potassium triggers inflammatory bowel disease via the inhibition of focal adhesion pathway.

Acesulfame potassium (ACK) was generally regarded as innocuous and extensively ingested. Nevertheless, ACK has recently gained attention as a burgeoning pollutant that has the potential to induce a range of health hazards, particularly to the digestive system. Herein, we uncover that ACK initiates inflammatory bowel disease (IBD) in mice and zebrafish, as indicated by the aggregation of macrophages in the intestine and the inhibition of intestinal mucus secretion. Transcriptome analysis of mice and zebrafish guts revealed that exposure to ACK typically impacts the cell cycle, focal adhesion, and PI3K-Akt signaling pathways. Using pharmacological approaches, we demonstrate that the PI3K-Akt signaling pathway and the generation of reactive oxygen species (ROS) triggered by cell division are not significant factors in the initiation of IBD caused by ACK. Remarkably, inhibition of the focal adhesion pathway is responsible for the IBD onset induced by ACK. Our results indicate the detrimental impacts and possible underlying mechanisms of ACK on the gastrointestinal system and provide insights for making informed choices about everyday dietary habits.

Modified ASO conjugates encapsulated with cytidinyl/cationic lipids exhibit more potent and longer-lasting anti-HCC effects.

Antisense oligonucleotides (ASOs) are a class of therapeutics targeting mRNAs or genes that have attracted much attention. However, effective delivery and optimal accumulation in target tissues in vivo are still challenging issues. CT102 is an ASO that targets IGF1R mRNA and induces cell apoptosis. Herein, a detailed exploration of the tissue distribution of ASOs delivered by liposomes was carried out. A formulation that resulted in increased hepatic accumulation was identified based on multiple intermolecular interactions between DCP (cytidinyl/cationic lipid DNCA/CLD and DSPE-PEG) and oligonucleotides, including hydrogen bonding, π-π stacking, and electrostatic interactions. The structurally optimized CT102s present a novel strategy for the treatment of hepatocellular carcinoma. The gapmer CT102MOE5 and conjugate Glu-CT102MOE5 showed superior antiproliferation and IGF1R mRNA suppression effects at 100 nM in vitro and achieved greater efficacy at a lower dose and administration frequency in vivo. Combined transcriptome and proteome analyses revealed that additional associated targets and functional regulations might simultaneously exist in ASO therapy. These results showed that a combination of lipid encapsulation and structural optimization in the delivery of oligonucleotide drugs has favorable prospects for clinical application.

Loss of miR-637 promotes cancer cell stemness via WASH/IL-8 pathway and serves as a novel prognostic marker in esophageal squamous cell carcinoma.

BACKGROUND: Esophageal carcinoma is the highly lethal cancer in the world, predominantly in some areas of East Asia. We previously reported that overexpression of cytoskeleton regulator Wiskott-Aldrich syndrome protein and SCAR Homolog (WASH) associates with poor prognosis of patients with esophageal squamous cell carcinoma (ESCC). However, the molecular mechanism and clinical significance involved in WASH overexpression have not been fully elucidated. METHODS: Bioinformatics analysis and luciferase reporter assay were used to predict and validate miR-637 as a regulator of WASH in ESCC cell lines. qRT-PCR, Western blotting and ELISA assays were performed to examine RNA expression and protein levels, respectively. Next, the biological functions of miR-637 were explored by tumor sphere formation assay in vitro and nude mouse tumor xenograft in vivo. Finally, we evaluated the association of miR-637 levels with clinical features in ESCC patients. RESULTS: We identified miR-637 as a WASH-targeting miRNA. miR-637 mimic strongly attenuated the downstream IL-8 production and tumor sphere formation in esophageal cancer cells, whereas miR-637 inhibitor displayed an opposite effect. IL-8 could facilitate stem-like properties and partially rescue the phenotypes induced by miR-637 mimic. Furthermore, miR-637 inhibitor dramatically promoted IL-8 expression and cancer stemness properties in a WASH-dependent manner. Ectopic expression of miR-637 also inhibited tumor growth in a mouse model. Clinically, low expression of miR-637 was observed in tumor tissues and the low expression levels of miR-637 were correlated with poor survival of ESCC patients. In particular, plasma miR-637 could be used as a noninvasive biomarker for ESCC patients. CONCLUSIONS: These results implicate the potential application of miR-637 for diagnosis and prognosis of esophageal cancer.

An Empirical Study on the Promotion of Students' Physiological and Psychological Recovery in Green Space on Campuses in the Post-Epidemic Era.

Human health is closely related to the environment; a relaxing and pleasant landscape environment can make people feel less stressed and more energetic. To investigate the restorative potential of landscape types and landscape elements in the post-epidemic era from the perspective of visual perception, this study selected Sichuan Agricultural University's Laoban hill, Jiuqu bridge, and the ginkgo garden to carry out physiological and psychological measurement experiments with college students. Research results on the psycho-biological and perceptual recovery vary with the types of landscape spaces. The results of the physiological data showed that all three space types had no significant effect on the recovery of blood pressure and heart rate; Laoban hill and Jiuqu bridge had some impact on concentration, while the ginkgo garden had no significant effect; and all three space types had some effect on the relaxation of the subjects' mental state. The results of the psychological data showed that the subjects' emotions were significantly improved in the three different landscape space types. The space with the strongest restorative effect on negative emotions was the ginkgo garden, followed by Jiuqu bridge and Laoban hill. The spaces with the strongest restorative potential for positive emotions were Jiuqu bridge and the ginkgo garden, followed by Laoban hill. The results of the perceptual restoration data showed that the Laoban hill space had the most effective restorative potential on the human body, followed by Jiuqu bridge, with the ginkgo garden having the least effective restorative potential. The results of the study on the difference between the aesthetic preference of different landscape elements and the perception restorative effect of a space showed that "the harmony between artificial structures such as garden pieces and the environment", "plant species", "waterscape state", and "boundary clarity" were identified as significant landscape elements with perception-restorative effects. These findings summarize campus landscape types and elements with optimal restorative potential. In the future, in campus landscape design-an active approach with a scientific combination and configuration of campus landscape types and elements-can provide a feasible solution to enhance the potential of campus landscape restorative effects.

Free thyroxine level is associated with both relapse rate and poor neurofunction in first-attack Neuromyelitis Optica Spectrum Disorder (NMOSD) patients.

BACKGROUND: To investigate whether the serum free thyroxine (FT4) level is a prognostic factor for the first-attack neuromyelitis optica spectrum disorders (NMOSD). METHODS: This retrospective study enrolled 109 patients with first-attack NMOSD. The Expanded Disability Status Scale (EDSS) and the relapse rate were used to evaluate the outcomes. The logistic regression model was used to analyze the independent effects of FT4 on relapse and final EDSS. Kaplan-Meier analysis, scatter plot smoothing method, and two-phase piecewise linear regression model were used to investigate the relationship between the FT4 level and the relapse rate. RESULTS: Multivariate analysis revealed that serum FT4 level might be a risk factor for both final EDSS (ß = 0.17; 95% confidence interval: 0.03-0.32) and the relapse rate (HR = 1.18; 95% confidence interval: 1.05-1.32). Furthermore, 1400 days after the onset, nearly 100% of patients in the high-FT4 group relapsed, while only 40% of the patients in the low-FT4 group relapsed. Finally, we found that the relationship between the FT4 level and the NMOSD relapse rate was nonlinear. The risk of NMOSD relapse increased with the FT4 level up to the inflection point of 12.01 pmol/L (HR = 1.45; 95% confidence interval: 1.06-1.98). When the FT4 level was > 12.01 pmol/L, there was no correlation between the FT4 level and the risk of NMOSD relapse (HR = 1.05; 95% confidence interval: 0.78-1.41). CONCLUSION: Serum FT4 level may be a prognostic indicator for the first-attack in patients with NMOSD. High FT4 levels are associated with poor neurofunctions and a high relapse rate in patients with the first-attack in patients with NMOSD.

Triglyceride Level Is an Independent Risk Factor in First-Attacked Neuromyelitis Optica Spectrum Disorders Patients.

Objective: To investigate prospective associations between triglyceride (TG) level and prognosis of first-attacked patients with neuromyelitis optica spectrum disorders (NMOSD). Methods: This retrospective study included 196 patients newly diagnosed with NMOSD from June 2014 to December 2018. Data of clinical parameters, including age of onset, sex, BMI, blood lipid levels, anti-aquaporin-4 status, serum glucose level, therapy regimens, comorbidities, initial Expanded Disability Status Scale (EDSS), relapses, and outcomes were collected. We used logistic regression models to examine the associations among relevant clinical factors and outcomes, and statistical analyses were performed using the SPSS 23.0 software. Results: Compared with the high TG group, residual EDSS was relatively lower in the normal TG group (median 1.0 vs. 2.0, P = 0.002). In the univariate analysis, TG level was positively correlated with outcomes (OR 1.75, 95% CI 1.18-2.60, P = 0.005) and relapses (OR 1.57, 95% CI 1.07-2.31, P = 0.02). Our stratified analysis suggested that patients with normal BMI (OR 4.90, 95% CI 2.10-11.44, P = 0.001) were closely correlated with poor recovery owing to increased TG level. In the multivariate analysis, a statistically significant association still existed between TG level and outcomes (OR 3.44, 95% CI 1.02-11.64; P = 0.040) after adjusting for various variables. Conclusions: In first-attacked NMOSD patients, TG level was positively associated with poor recovery. Early monitoring and treatment of elevated TG level in NMOSD patients are important.

MicroRNA-181 inhibits glioblastoma cell growth by directly targeting CCL8.

MicroRNAs (miRNAs/miRs), including miR-181, are closely linked to the development and progression of glioblastoma. However, the function of miR-181 in glioblastoma has not been fully clarified. The aim of the present study was to investigate the role of miR-181 in glioblastoma. miR-181 was revealed to be downregulated in glioblastoma tissues and cell lines, and associated with poor prognosis in patients with glioblastoma. Overexpression of miR-181 inhibited glioblastoma cell proliferation, invasion and migration, arrested glioblastoma cell cycle in the G1 phase and induced glioblastoma cell apoptosis. miR-181 was demonstrated to decrease expression of C-C motif chemokine ligand 8 (CCL8) by directly interacting with its 3'-untranslated region. Overexpression of CCL8 inversely reversed the proliferation, invasion and migration-promoting effects of miR-181 in glioblastoma cells. Furthermore, CCL8 was upregulated in glioblastoma tissues and was negatively correlated with miR-181 expression. These results indicate that miR-181 is a potential molecular biomarker or therapeutic target in the clinical management of glioblastoma.

The R132H mutation in IDH1 promotes the recruitment of NK cells through CX3CL1/CX3CR1 chemotaxis and is correlated with a better prognosis in gliomas.

Mutations in the isocitrate dehydrogenase (IDH) 1 gene, especially the R132H mutation, have been reported to be associated with a better prognosis in glioma patients. However, the underlying molecular mechanisms are not yet well understood. Many factors may contribute to differences in the survival of IDH1 wild-type and IDH1 mutant glioma patients, in which immune components play a potentially important role. In this study, we analyzed The Cancer Genome Atlas (TCGA), and the Chinese Glioma Genome Atlas (CGGA) databases, as well as glioma patient-derived tumor samples. We found that there was a higher infiltration of natural killer (NK) cells in IDH1 mutant glioma patients, and this was correlated with a better prognosis. We also showed that IDH1-R132 tumor cells had higher expression levels of the chemokine CX3CL1. This arises as a result of the conversion of α-ketoglutarate to R(-)-2-hydroxyglutarate by the IDH1 mutant and the resultant phosphorylation of nuclear factor kappa B. Knockdown of CX3CL1 decreased the migration of NK cells. In addition, the high levels of expression of CX3CL1 were positively correlated with glioma patient survival in the TCGA and CGGA databases, and in the clinical samples. Overall, our data have identified a novel mechanism in which R132H mutation of the IDH1 gene serves as a tumor suppressor by promoting the recruitment of NK cells through CX3CL1/CX3CR1 chemotaxis.

Th17 cell-derived IL-17A promoted tumor progression via STAT3/NF-κB/Notch1 signaling in non-small cell lung cancer.

Non-small cell lung cancer (NSCLC) accounts for the majority of all lung cancer cases, which is the leading cause of cancer deaths worldwide. IL-17░A, the major effector cytokine derived from Th17 cells, is a key cytokine in tumor pathogenesis and modulates tumor progression. We aimed to identify whether IL-17░A derived from Th17 cells promotes the progression of NSCLC. Here we found that the level of Th17 cells was increased in NSCLC and IL-17░A was mainly produced by CD4+ cells (Th17 cells) in NSCLC. IL-17░A enhanced the migration, invasion and stemness of NSCLC via STAT3/NF-κB/Notch1 signaling. Blockade of this signaling inhibited the migration, invasion and stemness of NSCLC mediated by IL-17░A. Th17 cells in NSCLC were closely associated with poor prognosis of NSCLC patients. Our results indicated that Th17 cell-derived IL-17░A plays an important role in tumor progression of NSCLC via STAT3/NF-κB/Notch1 signaling. Therefore, therapeutic strategies against this pathway would be valuable to be developed for NSCLC treatment.

Large-scale analysis reveals the specific clinical and immune features of B7-H3 in glioma.

Background: B7-H3 is an immune checkpoint member that belongs to B7-CD28 families and plays a vital role in the inhibition of T-cell function. Importantly, B7-H3 is widely overexpressed on solid tumors, making it become an attractive target for cancer immunotherapy. To clarify the expression panel of B7-H3 in glioma, we explored the clinical and immune features of B7-H3 expression in a large-scale study. Methods and patients: Totally, 1323 glioma samples from Chinese Glioma Genome Atlas (CGGA) dataset, including 325 RNAseq data and 301 mRNA microarray data, and The Cancer Genome Atlas (TCGA) dataset, including 697 RNAseq data, were gathered into our research. The statistical analysis and graphical work were mainly realized by R language. Results: B7-H3 expression was found positively correlated with the grade of malignancy, which might be caused by hypomethylation. The expression level of B7-H3 was consistently up-regulated in IDH wild-type glioma and highly enriched in mesenchymal subtype. GSEA analysis suggested that B7-H3 related genes were more involved in immune response and angiogenesis in glioma. Moreover, B7-H3 showed a consistent positive relationship with stromal and immune cell populations. Further analysis confirmed that B7-H3 played an important role in T-cell-mediated immunity, especially in T-cell-mediated immune response to tumor cell. Circos plots revealed that B7-H3 was tightly associated with most B7 members and other immune checkpoints. Univariate and multivariate cox analysis demonstrated that B7-H3 was an independent prognosticator for glioma patients. Conclusion: B7-H3 represents the malignant phenotype of glioma and independently predicted worse prognosis in glioma patients. Moreover, B7-H3 collaborating with other checkpoint members may contribute to the dysfunctional phenotype of T cell. These findings will be helpful for further optimizing immunotherapies for glioma.

Interleukin 8 (CXCL8)-CXC chemokine receptor 2 (CXCR2) axis contributes to MiR-4437-associated recruitment of granulocytes and natural killer cells in ischemic stroke.

Granulocytes and natural killer (NK) cells have been linked to brain injury in ischemic stroke. However, their recruitment from peripheral leucocytes in stroke patients is not well understood. Here, the expression of the interleukin 8 (CXCL8) in plasma, and CXC chemokine receptor 2 (CXCR2) in peripheral leucocytes of patients with ischemic stroke were evaluated. Based on the results, CXCR2 expression positively correlated with granulocytes and NK cells, which were in turn attracted by CXCL8. The results also indicated that CXCR2 was a direct target of microRNA (miR)-4437, a negative regulator of CXCR2, which was downregulated in peripheral leucocytes from patients with ischemic stroke. Furthermore, serum CXCL8 levels were associated with the infarct volume and functional outcomes in patients with ischemic stroke. The results of the receiver operating characteristic curve analysis with an optimal cut-off value of 34 pg/mL indicated serum CXCL8 levels could be a prognostic indicator for ischemic stroke. In conclusion, these data highlighted the involvement of the CXCL8-CXCR2 chemotactic axis in the recruitment of granulocytes and NK cells in ischemic stroke. Furthermore, miR-4437 was suggested as a novel target for treating ischemic stroke, while the serum CXCL8 level could be a prognostic factor for ischemic stroke.

Metformin-Induced Reduction of CD39 and CD73 Blocks Myeloid-Derived Suppressor Cell Activity in Patients with Ovarian Cancer.

Metformin is a broadly prescribed drug for type 2 diabetes that exerts antitumor activity, yet the mechanisms underlying this activity remain unclear. We show here that metformin treatment blocks the suppressive function of myeloid-derived suppressor cells (MDSC) in patients with ovarian cancer by downregulating the expression and ectoenzymatic activity of CD39 and CD73 on monocytic and polymononuclear MDSC subsets. Metformin triggered activation of AMP-activated protein kinase α and subsequently suppressed hypoxia-inducible factor α, which was critical for induction of CD39/CD73 expression in MDSC. Furthermore, metformin treatment correlated with longer overall survival in diabetic patients with ovarian cancer, which was accompanied by a metformin-induced reduction in the frequency of circulating CD39+CD73+ MDSC and a concomitant increase in the antitumor activities of circulating CD8+ T cells. Our results highlight a direct effect of metformin on MDSC and suggest that metformin may yield clinical benefit through improvement of antitumor T-cell immunity by dampening CD39/CD73-dependent MDSC immunosuppression in ovarian cancer patients.Significance: The antitumor activity of an antidiabetes drug is attributable to reduced immunosuppressive activity of myeloid-derived tumor suppressor cells. Cancer Res; 78(7); 1779-91. ©2018 AACR.

miR-29a-3p suppresses cell proliferation and migration by downregulating IGF1R in hepatocellular carcinoma.

Hepatocellular carcinoma (HCC), the most common primary tumor of the liver, has a poor prognosis and rapid progression. MicroRNAs (miRNAs) play important roles in carcinogenesis and tumor progression. Insulin-like growth factor 1 receptor (IGF1R) is a transmembrane heterotetrameric protein that has been reported to promote transformation to malignancy and cancer cell proliferation and survival. In this study, we found that the expression of miR-29a-3p was downregulated in HCC patients, resulting in poor survival rates. Contrastingly, the overexpression of miR-29a-3p significantly inhibited proliferation and migration in HepG2 cells. miR-29a-3p directly targeted IGF1R and down-regulated its expression. Moreover, knockdown of IGF1R led to the increased production of chemokine ligand 5 (CCL5). In tumor lesions, the local expression of CCL5 negatively affected the expression of IGF1R. Transwell analysis showed that CCL5 was important for the chemotactic movement of CD8+ T lymphocytes. The expression of CCL5 in HCC tissues positively correlated with the expression of CD8+ T lymphocyte surface marker, CD8. Patients with high CCL5 expression exhibited better survival. Our results revealed that miR-29a-3p is a tumor suppressor gene that acts by directly repressing the oncogene IGF1R, which takes part in immunoregulation in tumor microenvironments in HCC, implying that miR-29a-3p could be a potential target for HCC treatment.

A meta-analysis of flexible intramedullary nailing versus external fixation for pediatric femoral shaft fractures.

To compare the difference in efficacy following flexible intramedullary nailing (FIN) and external fixation (EF) for pediatric femoral shaft fractures. A systematic search was performed on PubMed, Embase, Medline, and Cochrane library for relevant studies. We included controlled trials comparing complications between FIN and EF for pediatric femoral shaft fractures published before 25 November 2014. Modified Jadad scores were utilized to assess the methodological quality of the studies included. The meta-analysis was carried out using Stata 12.0 software. Six studies involving 237 patients were included. On comparison of EF, a low incidence of overall complications [relative risk (RR)=0.30, 95% confidence interval (CI): 0.19-0.46; P<0.001] and pin-tract infection (RR=0.286, 95% CI: 0.13-0.61; P=0.001), but a high risk of soft tissue irritation (RR=1.86, 95% CI: 1.35-2.56; P<0.001) were found in patients treated with the FIN approach. No significant differences in other complications were found. On the basis of current evidence, the use of FIN leads to fewer complications than EF and may be considered as the first-line approach in the treatment of femoral shaft fractures.

Study on the clinical efficacy of Human Urinary Kalllikrein in the treatment of acute cerebral infarction according to TOAST classification.

To observe and evaluate the clinical efficacy of Human Urinary Kallikrein in the treatment of acute cerebral infarction (ACT) according to TOAST (The Trial of Org 10172 in Acute Stroke Treatment) classification. In accordance with randomized controlled trial, 110 patients with acute cerebral infarction were randomly assigned to kallikrein treatment group (55 cases) and control group (55 cases). TOAST classification and basic treatment were administrated on patients between two groups respectively. 0.15 PNA unit of Human Urinary Kallikrein injection plus 100 mL saline in intravenous infusion was performed in the kallikrein group, with once a day for 14 consecutive days. The National Institutes of Health Stroke Scale (NIHSS) scores in two groups were analyzed before and after the treatment. No difference was shown in the NIHSS scores before treatment among patients between two groups (P>0.05). While after the treatment, the NIHSS scores in both groups were reduced (P<0.05) and the NIHSS scores in the kallikrein treatment group were less than those in control group (P<0.05). Moreover, after the treatment, the NIHSS scores for large-artery atherosclerosis subtype (L) and small-artery occlusion lacunar subtype (S) as two subtypes of TOAST classification in the two groups were both reduced (P<0.05). After the treatment, NIHSS scores for L subtype in the kallikrein treatment were less than those in the control group (P<0.05). After the treatment, NIHSS scores for S subtype in the kallikrein treatment were less than those in the control group, without statistically significant difference. Comparisons on clinical efficacy indicated differences on the S subtype between two groups (P<0.05). The standardization effective rate was calculated, indicating 81.82% in the kallikrein treatment group and 54.55% in the control group, respectively. In TOAST classification, Human Urinary Kallikrein is able to remarkably improve the NIHSS scores for L subtype and S subtype patients with acute cerebral infarction and help to enhance the clinical efficacy.

MicroRNA let-7e regulates the expression of caspase-3 during apoptosis of PC12 cells following anoxia/reoxygenation injury.

This study aimed to investigate the role and mechanism of action of microRNA (miR) let-7e in PC12 cells undergoing apoptosis following anoxia/reoxygenation (A/R) injury. The putative binding site of let-7e in the 3' UTR of caspase-3 (Casp3) mRNA was analyzed using the miRanda algorithm. Precursor let-7e (pre-miRNA), let-7e miR and anti-let-7e oligonucleotides were transfected into PC12 cells, which were then subjected to A/R injury. The levels of Casp3 mRNA and let-7e miRNA, the total protein levels of Casp3, Casp8 and Casp9 and levels of cellular apoptosis were measured. It was found that let-7e expression in PC12 cells was decreased, whereas the expression of Casp3 was significantly increased after A/R injury. The transfection of pre-miRNA or let-7e miR into PC12 cells decreased Casp3 expression levels and cellular apoptosis following A/R injury, while co-transfection of anti-let-7e strikingly alleviated the effects of let-7e miR. These results indicate that let-7e may protect PC12 cells against apoptosis following A/R injury by negatively regulating the expression of Casp3.

[Interaction of microRNA-338 and its potential targeting protein eiF4E3].

OBJECTIVE: To analyze the interaction between the microRNA-338 and its targeting proteins during the cerebral ischemia and reperfusion injury. METHODS: TargetScan was used to predict the targets of microRNA-338. The potential targeting proteins were then selected according to their secondary structures using RNA structure 4.6 software and their involvement in cerebral ischemia and reperfusion injury was studied. Dual-luciferase reporter assay was used to testify whether microRNA-338 can recognize the 3'UTR of target protein. Western blot was applied to analyze the expression of eiF4E3 in both experimental group and control group. RESULT: EiF4E3 was the most likely potential targeting protein of microRNA-338. The secondary structure of local region of eiF4E3 recognizing microRNA-338 was conservative. The ratio of firefly to renilla luciferase activity in the experimental group was much higher than that of control group. However, there was no significant difference in the expression of eiF4E3 between these two groups. CONCLUSION: MicroRNA-338 can recognize the 3'UTR of eiF4E3 while it has no significant effect on the expression of eiF4E3. The post-target-recognizing regulation for miRNA do exist and this mechanism is possibly related to the tertiary structure of target mRNA.