Investigation of Spatial Orientation and Kinetic Energy of Reactive Site Collision between Benzyl Chloride and Piperidine: Novel Insight into the Microwave Nonthermal Effect.

Microwave nonthermal effect in chemical reactions is still an uncertain problem. In this work, we have studied the spatial orientation and kinetic energy of reactive site collision between benzyl chloride and piperidine molecules in substitution reaction under microwave irradiation using the molecular dynamics simulation. Our results showed that microwave polarization can change the spatial orientation of reactive site collision. Collision probability between the Cl atom of the C-Cl group of benzyl chloride and the H atom of the N-H group of piperidine increased by up to 33.5% at an effective spatial solid angle (θ, φ) of (100∼110°, 170∼190°) under microwave irradiation. Also, collision probability between the C atom of the C-Cl group of benzyl chloride and the N atom of the N-H group of piperidine also increased by up to 25.6% at an effective spatial solid angle (θ, φ) of (85∼95°, 170∼190°). Moreover, the kinetic energy of collision under microwave irradiation was also changed, that is, for the collision between the Cl atom of the C-Cl group and the H atom of the N-H group, the fraction of high-energy collision greater than 6.39 × 10-19 J increased by 45.9 times under microwave irradiation, and for the collision between the C atom of the C-Cl group and the N atom of the N-H group, the fraction of high-energy collision greater than 6.39 × 10-19 J also increased by 29.2 times. Through simulation, the reaction rate increased by 34.4∼50.3 times under microwave irradiation, which is close to the experimental increase of 46.3 times. In the end, spatial orientation and kinetic energy of molecular collision changed by microwave polarization are summarized as the microwave postpolarization effect. This effect provides a new insight into the physical mechanism of the microwave nonthermal effect.

Downregulation of microRNA-103a reduces microvascular endothelial cell injury in a rat model of cerebral ischemia by targeting AXIN2.

Multiple microRNAs (miRNAs) have been found to be linked with cerebral ischemia. Thus, this study was employed to characterize the capabilities of miRNA-103a (miR-103a) on the brain microvascular endothelial cells (BMECs) injury in rat models of middle cerebral artery occlusion (MCAO) by regulating AXIN2. The MCAO rat model was developed by the suture method, where normal saline, miR-103a inhibitors, or its negative control were separately injected into the lateral ventricle to assess the function of miR-103a inhibitors in BMECs apoptosis, microvessel density, as well as angiogenesis. In addition, the oxygen-glucose deprivation model was induced in primarily cultured BMECs to unearth the functions of miR-103a inhibitors on cell viability and apoptosis, lactate dehydrogenase (LDH) release and tube formation ability. Furthermore, the relationship between miR-103a and AXIN2 was verified. The modeled rats of MCAO showed robustly expressed miR-103a, poorly expressed AXIN2, severe neurological deficits, accelerated apoptosis and reduced angiogenesis. miR-103a expression had a negative correlation with AXIN2 messenger RNA expression (r = -0.799; p < .05). In response to the treatment of miR-103a inhibitors, the BMECs apoptosis was suppressed and angiogenesis was restored, corresponding to upregulated Bcl-2, VEGF, and Ang-1, in addition to downregulated caspase-3 and Bax. Meanwhile, AXIN2 was verified to be the miR-103a's target gene. More important, miR-103a inhibitors led to promoted BMEC viability and tube formation and suppressed apoptosis and LDH release rate. This study highlights that miR-103a targets and negatively regulates AXIN2, whereby reducing BMEC injury in cerebral ischemia.

MTA1 promotes viability and motility in nasopharyngeal carcinoma by modulating IQGAP1 expression.

Nasopharyngeal carcinoma (NPC) is frequently seen in Chinese, especially the population that resides in southeast China. Metastasis-associated protein 1 (MTA1) is a chromatin modifier and plays a role in tumor cell metastasis. IQGAP1 is a ubiquitously expressed protein that contributes to cytoskeleton remodeling. This study aimed to investigate the role of MTA1 and IQGAP1 in NPC malignant transformation. MTA1 and IQGAP1 expression in NPC (n = 43) and control tissues (n = 31) were detected using qRT-PCR, immunoblot, and immunohistochemistry. MTA1 was overexpressed in CNE-1 and CNE-2 cell line by pcDNA3.1/MTA1 transfection. Dominant-negative p53 was transfected to inhibit p53 activity. si-IQGAP1 or dominant-negative IQGAP1 (IQGAP1ΔGRD) was used to suppress IQGAP1 activity. Cell proliferation was measured by CKK-8 assay. Cell migration was evaluated by Transwell assay. The results showed that MTA1 and IQGAP1 were highly expressed in NPC tissues compared with the controls. Forced expression of MTA1 accelerated cell proliferation and migration and upregulated IQGAP1 expression in a p53-independent way. Knockdown of IQGAP1 or transfection of dominant-negative IQGAP1 impeded tumor cell proliferation and migration as well as PI3K/Akt signaling induced by MTA1. In conclusion, MTA1 participates in NPC malignant transformation via regulating IQGAP1 expression and PI3K/Akt signaling pathway.

EZH2 promotes cell proliferation by regulating the expression of RUNX3 in laryngeal carcinoma.

Enhancer of zeste homolog 2 (EZH2) is a highly conserved histone methyltransferase, which is overexpressed in different types of cancers such as breast and prostate cancer. It is reported that EZH2 can directly down-regulate RUNX3 by increasing histone H3 methylation. However, the role of EZH2 in the development and progression of laryngeal carcinoma has not yet been investigated, and the relationship between EZH2 and RUNX3 in laryngeal carcinoma is rarely reported. The current study aims to determine the role of EZH2 in the progression of laryngeal carcinoma, and investigate the interaction between EZH2 and the tumor suppressor RUNX3. Our study found that EZH2 is overexpressed in laryngeal carcinoma patients, and silencing EZH2 by EZH2 siRNA significantly inhibited the proliferation of laryngeal carcinoma cells. Besides, we also found that RUNX3 is repressed in laryngeal carcinoma patients. Moreover, RUNX3 as a downstream target protein of EZH2 is up-regulated by EZH2 siRNA accompanied by a decrease in the trimethylation modification pattern of H3K27. RUNX3 siRNA inhibits the decreased proliferation induced by EZH2 siRNA. Furthermore, ß-catenin protein expression is down-regulated by EZH2 siRNA and up-regulated by RUNX3 siRNA, and RUNX3 siRNA inhibits the down-regulation effect of EZH2 siRNA on ß-catenin protein expression. Additionally, the Wnt/ß-catenin activator BIO reverses the inhibitory effect of EZH2 siRNA on Hep-2 cell proliferation. Taken together, our results suggest that EZH2 regulates cell proliferation potentially by targeting RUNX3 through the Wnt/ß-catenin signaling pathway in laryngeal carcinoma.

MicroRNA-26a inhibits proliferation and tumorigenesis via targeting CKS2 in laryngeal squamous cell carcinoma.

Laryngeal squamous cell carcinoma (LSCC) is one of the most common head and neck cancers, with high mortality and incidence. MicroRNA-26a (miR-26a) is involved in the development and progression of several tumours. However, the roles of miR-26a and its target CKS2 in LSCC progression are not yet clear. The mRNA and protein expression was determined using RT-PCR and Western blotting assay, respectively. Cell proliferation was detected using a Cell Counting kit-8 assay (CCK-8). Transwell assay was used to evaluate cell migration and invasion. Dual-luciferase reporter assay was applied to determine the relationship between miR-26a and CKS2. In addition, a tumour xenograft model in nude mice was established to further determine the effects of miR-26a on tumourigenesis. In this study, we found that miR-26a level was down-regulated in LSCC tissues and cell lines, while CKS2 expression was increased. Cell proliferation, migration, invasion and the expression of MMP2 and MMP9 was suppressed by miR-26a overexpression, but enhanced by inhibition of miR-26a. Dual-luciferase reporter assay demonstrated that CKS2 is a direct target of miR-26a in AMC-HN-8 cells. Overexpression of miR-26a caused a significant reduction in CKS2 expression, and reinforced expression of CKS2 abolished the tumour-suppressive function of miR-26a. Moreover, miR-26a inhibited tumour growth in vivo. Taken together, miR-26a inhibited proliferation and tumourigenesis of LSCC via targeting CKS2 in vitro and in vivo.

MiR-503 enhances the radiosensitivity of laryngeal carcinoma cells via the inhibition of WEE1.

Enhancing the sensitivity of laryngeal cells to radiation is crucial for improving the efficacy of laryngeal carcinoma. MicroRNAs are known to play a major role in regulating cellular radiosensitivity. This study was designed to explore the effect and the molecular basis of miR-503 in the radiosensitivity of laryngeal carcinoma cells. Quantitative real-time polymerase chain reaction analysis showed that miR-503 expression was decreased in human laryngeal carcinoma cell lines Hep-2 and TU212, and the downregulation of miR-503 was also observed after irradiation. Upregulation of miR-503 by pre-miR-503 transfection restrained proliferation, promoted progression of Hep-2 and TU212 cells through the cell cycle after irradiation, and sensitized cells to radiation. Dual-Luciferase Reporter Assay verified a direct interaction between miR-503 and the WEE1 messenger RNA 3'-untranslated region. The overexpression of miR-503 significantly decreased WEE1 expression at the messenger RNA and protein levels, whereas the inhibition of miR-503 upregulated the expression of WEE1. WEE1 knockdown by WEE1 small interfering RNA apparently abrogated the inhibitory effect of anti-miR-503 on radiosensitivity. In conclusion, miR-503 could function as an enhancer of radiation responses in laryngeal carcinoma cells by inhibiting WEE1, which may be a potential novel radiosensitizing strategy for laryngeal carcinoma.

Enantioselective synthesis of spiro[indoline-3,4'-pyrano[2,3-c]pyrazole] derivatives via an organocatalytic asymmetric Michael/cyclization cascade reaction.

An efficient enantioselective synthesis of spiro[indoline-3,4'-pyrano[2,3-c]pyrazole] derivatives by a cascade reaction between pyrazolones and isatylidene malononitriles is described. With only 1 mol% of (DHQD)2PYR, chiral spirooxindole derivatives have been produced in excellent yields (96-99%) with good-to-excellent enantioselectivities (up to 91% ee).

Release of feruloylated oligosaccharides from wheat bran through submerged fermentation by edible mushrooms.

Wheat bran, a by-product of the flour industry, is believed to be a raw material for the production of feruloylated oligosaccharides (FOs) because of its high content of conjiont ferulic acid (FA). Studies were carried out to identify edible mushrooms that are able to release FOs from wheat bran. All the six tested mushrooms (Pleurotus ostreatus, Hericium erinaceum, Auricularia auricula, Cordyceps militaris, Agrocybe chaxingu, and Ganoderma lucium) were found to release FOs, and Agrocybe chaxingu had the highest yield, reaching 35.4 µM in wheat bran broth. Enzymes detection showed that these species secreted extracellular enzymes during fermentation, including cellulase and xylanase. Agrocybe chaxingu secreted the significant amount of xylanase (180 mU ml(-1) ), which was responsible for the release of FOs from wheat bran, while Hericium erinaceum secreted FA esterase which could disassemble FOs.

Bioinformatics analysis and experimental validation revealed that Paeoniflorigenone effectively mitigates cerebral ischemic stroke by suppressing oxidative stress and inflammation.

Inflammation and oxidative stress are becoming more recognized as risk factors for ischemic stroke. Paeoniflorigenone (PA) has diverse pharmacological effects that include anti-inflammatory and antioxidant properties. However, the specific mechanisms by which PA affects cerebral ischemic stroke have not been studied. Our objective was to investigate the potential targets and mechanisms of PA in preventing cerebral ischemic stroke. We obtained the potential targets of PA from the SwissTargetPrediction, Super-PRED, and SEA Search Server databases. The GSE97537 dataset was utilized to identify gene targets related to ischemic stroke. The overlapping targets were imported into the STRING database to construct a protein-protein interaction network, and enrichment analyses were conducted using R software. Rats were pretreated with PA for three weeks before undergoing MCAO and reperfusion. H&E staining, ELISA, and qRT-PCR analyses were then performed to explore the potential mechanisms of PA. In the study, we identified 439 potential targets for PA and 1206 potential targets for ischemic stroke. Out of these, there were 71 common targets, which were found to be primarily associated with pathways related to oxidative stress and inflammation. The results from animal experiments showed that PA was able to improve nerve function and reduce inflammatory cytokines and oxidative stress in the MCAO-induced ischemic stroke model. Additionally, the expression of core genes in the MCAO + HPA group was significantly lower compared to the MCAO group. Our study revealed that the potential mechanisms by which PA prevents ischemic stroke involve oxidative stress and inflammation. These findings provide important theoretical guidance for the clinical use of PA in preventing and managing ischemic stroke.

Cost-effectiveness of incorporating self-imaging optical coherence tomography into fundus photography-based diabetic retinopathy screening.

Diabetic macular edema (DME) has emerged as the foremost cause of vision loss in the population with diabetes. Early detection of DME is paramount, yet the prevailing screening, relying on two-dimensional and labor-intensive fundus photography (FP), results in frequent unwarranted referrals and overlooked diagnoses. Self-imaging optical coherence tomography (SI-OCT), offering fully automated, three-dimensional macular imaging, holds the potential to enhance DR screening. We conducted an observational study within a cohort of 1822 participants with diabetes, who received comprehensive assessments, including visual acuity testing, FP, and SI-OCT examinations. We compared the performance of three screening strategies: the conventional FP-based strategy, a combination strategy of FP and SI-OCT, and a simulated combination strategy of FP and manual SD-OCT. Additionally, we undertook a cost-effectiveness analysis utilizing Markov models to evaluate the costs and benefits of the three strategies for referable DR. We found that the FP + SI-OCT strategy demonstrated superior sensitivity (87.69% vs 61.53%) and specificity (98.29% vs 92.47%) in detecting DME when compared to the FP-based strategy. Importantly, the FP + SI-OCT strategy outperformed the FP-based strategy, with an incremental cost-effectiveness ratio (ICER) of $8016 per quality-adjusted life year (QALY), while the FP + SD-OCT strategy was less cost-effective, with an ICER of $45,754/QALY. Our results were robust to extensive sensitivity analyses, with the FP + SI-OCT strategy standing as the dominant choice in 69.36% of simulations conducted at the current willingness-to-pay threshold. In summary, incorporating SI-OCT into FP-based screening offers substantial enhancements in sensitivity, specificity for detecting DME, and most notably, cost-effectiveness for DR screening.

The prognostic value of tumor-associated macrophages in glioma patients.

Glioma is a complex tumor composed of both neoplastic and non-neoplastic cells, including tumor-infiltrating leukocytes (TILs), and each cell type contributes to tumor formation and malignant progression. Among TILs, tumor-associated macrophages (TAMs) are of great importance and play a key role in the immune response to cancer. In this study, 22 types of adaptive and innate TILs were evaluated in gliomas. TAMs, which account for 38.7% of all these cells, are the most abundant immune infiltrates in the tumor microenvironment. In addition, we observed different immune cell patterns in low-grade glioma and glioblastoma. Our research indicated that there was a connection between TILs, and 13 of 22 TILs were significantly associated with patient outcomes. Finally, the prognosis and diagnostic value of TAMs were revealed using Kaplan-Meier analysis. We identified the optimal cutoff point of TAMs at an infiltrating level of 0.47 to predict patient prognosis, with a median overall survival of 448 days in patients with higher TAM infiltration levels and 2660 days in patients with lower TAM infiltration levels. These findings provide a new idea for glioma to regulate tumor-specific immunity, clarify the potential effects of TAMs on disease pathology, and provide a theoretical basis for immune intervention treatment of gliomas.

The circular RNA Ataxia Telangiectasia Mutated regulates oxidative stress in smooth muscle cells in expanding abdominal aortic aneurysms.

An abdominal aortic aneurysm (AAA) is a pathological widening of the aortic wall characterized by loss of smooth muscle cells (SMCs), extracellular matrix degradation, and local inflammation. This condition is often asymptomatic until rupture occurs, leading to high morbidity and mortality rates. Diagnosis is mostly accidental and the only currently available treatment option remains surgical intervention. Circular RNAs (circRNAs) represent a novel class of regulatory non-coding RNAs that originate from backsplicing. Their highly stable loop structure, combined with a remarkable enrichment in body fluids, make circRNAs promising disease biomarkers. We investigated the contribution of circRNAs to AAA pathogenesis and their potential application to improve AAA diagnostics. Gene expression analysis revealed the presence of deregulated circular transcripts stemming from AAA-relevant gene loci. Among these, the circRNA to the Ataxia Telangiectasia Mutated gene (cATM) was upregulated in human AAA specimens, in AAA-derived SMCs, and serum samples collected from aneurysm patients. In primary aortic SMCs, cATM increased upon angiotensin II and doxorubicin stimulation, while its silencing triggered apoptosis. Higher cATM levels made AAA-derived SMCs less vulnerable to oxidative stress, compared with control SMCs. These data suggest that cATM contributes to elicit an adaptive oxidative-stress response in SMCs and provides a reliable AAA disease signature.

Crafting Inconspicuous Luxury Brands Through Brand Authenticity in China.

Currently, we are witnessing a trend toward subtle or absent hints of luxury, reflecting the rise of inconspicuousness. We seek to address why and how Chinese luxury brand managers, instead of matching conspicuous branding of many Western brands, develop inconspicuous strategies and craft authentic attributes in their brand communication. In the Chinese luxury brand context, we use the ethnographic research method with in-depth interviews, field visits, and photographs of eight Chinese luxury brands with inconspicuous preferences to reveal three main themes contributing to inconspicuousness. First, an inconspicuous approach of Chinese luxury brands is derived from the rise of inconspicuous consumption in China and a rejection of status brands due to being less famous than well-known Western brands, superficiality of status branding, and limited production capability. Second, we argue that inconspicuous branding can encompass developing luxury brands that avoid overtly displaying wealth and social status. Third, we identify three ways of crafting brand authenticity to build inconspicuous brands by using (a) nature to craft quality commitment dimension of authenticity (places and rare raw materials); (b) traditional Chinese craftsmanship and symbols to craft heritage dimension of authenticity; and (c) sincere stories (of how innovations are used in traditional craftsmanship), and the use of sustainability (sustainable raw materials, traditional craftsmanship, luxury production process, and saving resources) to craft sincerity dimension of authenticity in developing inconspicuous brands.

The Impact of Algorithmic Price Discrimination on Consumers' Perceived Betrayal.

With the development of artificial intelligence technology, data support is increasing in importance, as are problems such as information disclosure, algorithmic discrimination and the digital divide. Algorithmic price discrimination occurs when online retailers or platforms charge experienced consumers who are purchasing products on their online platforms higher prices than those charged to new consumers for the same products at the same time. The purpose of this paper is to investigate the impact of algorithmic price discrimination on consumers' perceived betrayal. This paper employed a field experimental method involving two studies. In total, 696 questionnaires were distributed to consumers: 310 for Study 1 and 386 for Study 2. The collected data were analyzed using variance analysis and process analysis methods and SPSS software. Our findings suggest (1) Increased algorithmic price discrimination leads to increased perceived betrayal. (2) Increased algorithmic price discrimination leads to lower perceived price fairness and therefore to increased perceived betrayal among consumers. (3) Higher perceived ease of use of online retailers decreases the impact of algorithmic price discrimination on consumers' perceived betrayal. We are a small group of researchers focusing on algorithmic price discrimination and integrating algorithmic discrimination into the consumer research field. Our research introduces the concept of consumer perceived betrayal to the field of artificial intelligence. We adopt a field experimental study to examine the impact of algorithmic price discrimination on consumers' perceived betrayal by introducing variables of perceived price fairness and perceived ease of use.

Molecular Dynamics Research of Spatial Orientation and Kinetic Energy of Active Site Collision of Carnosine under Weak Microwave Irradiation.

The molecular mechanism of the microwave nonthermal effect is still not clear. This work investigated the spatial orientation and kinetic energy of active site collision of carnosine, a natural bioactive dipeptide, under the weak microwave irradiation using the molecular dynamics simulation. Our results showed the influences of the temperature, microwave intensity, microwave frequency, and microwave polarization mode (linear polarization and circular polarization) on the spatial orientation and kinetic energy of active site collision of carnosine. First, under the constant intensity and frequency of linear polarization microwave irradiation, the increment of the collision probability between the 6N atom of carnosine and the 28H atom of the other carnosine at effective space angle decreases from 85.0% to 3.5% with increasing temperature. Second, with the increase of microwave intensity, the change of spatial orientation and kinetic energy becomes more and more significant. However, the change of circular polarization microwaves on the spatial orientation and kinetic energy of collision is weaker than that of linear polarization. Third, under the constant intensity of linear polarization microwave irradiation, the collision probability between the 6N atom and the 28H atom at effective space angle decreases from 70.2% to 14.7% with increasing frequency. Finally, under the microwave polarization, the spatial orientation and kinetic energy of molecular collision are changed, which is summarized as the microwave postpolarization effect (MWPPE). The dependence of MWPPE on temperature, microwave intensity, microwave frequency, and polarization mode is very complicated. In the end, this effect can provide a new insight into the molecular mechanism of the microwave nonthermal effect.

Vappolotes, a new genus of coelotine spiders (Araneae, Agelenidae) from Guizhou, China.

A new genus of the subfamily Coelotinae F.O. Pickard-Cambridge, 1893, Vappolotes Zhao et S. Li gen. n., with two new species, V. ganlongensis Zhao et S. Li sp. n. (♂♀) and V. jianpingensis Zhao et S. Li sp. n. (♀), is described. The genus is restricted to southern China (Guizhou). Its relationship to other coelotine genera is discussed. A partial fragment of the mitochondrial cytochrome oxidase subunit I of both species were obtained to aid species identification at the molecular level.

New species of the coelotine spider genus Lineacoelotes (Araneae: Agelenidae) from China.

Four new species of Lineacoelotes Xu, Li Wang, 2008 are described from morphological features: L. lifengyuanae sp. n. (male and female) from Chongqing Municipality, and L. tiantaiensis sp. n. (female), L. zhongbaensis sp. n. (male and female), and L. ziboensis sp. n. (male and female) from Shaanxi Province, China.

Four new species of the genus Draconarius Ovtchinnikov, 1999 (Araneae, Agelenidae) from the Tibetan Plateau, China.

Four new species of Draconarius Ovtchinnikov, 1999 (Araneae, Agelenidae) from the Tibetan Plateau, China are described: Draconarius baibaensis sp. n. (♀), Draconarius budanlaensis sp. n. (♀), Draconarius yigongensis sp. n. (♂♀), and Draconarius yingbinensis sp. n. (♀). The male of Draconarius linzhiensis (Hu, 2001) is described for the first time and the female re-illustrated. All species belong to the Draconarius venustus-group. The examined specimens are deposited in the Institute of Zoology, Chinese Academy of Sciences (IZCAS) in Beijing.

Guilotes, a new genus of Coelotinae spiders from Guangxi Zhuang Autonomous Region, China (Araneae, Agelenidae).

A new genus of the subfamily Coelotinae F.O. Pickard-Cambridge, 1893, Guilotes Z. Zhao & S. Li, gen. n. from China is described, as well as four new species: G.ludiensis Z. Zhao & S. Li, sp. n. (♂♀, type species), G.qingshitanensis Z. Zhao & S. Li, sp. n. (♂♀), G.xingpingensis Z. Zhao & S. Li, sp. n. (♂♀) and G.yandongensis Z. Zhao & S. Li, sp. n. (♀). The DNA barcodes of all species are documented for future use.

MiR-340 impedes the progression of laryngeal squamous cell carcinoma by targeting EZH2.

Laryngeal squamous cell carcinoma (LSCC) is a common malignant tumor of the otolaryngeal region and accounts for 1-2% of all malignancies diagnosed worldwide. miR-340 down-regulation and EZH2 up-regulation have been frequently identified in multiple cancers, but the role of miR-340 and EZH2 in LSCC has not been explored. In this study, we investigated the regulative role of miR-340 in EZH2 expression and LSCC progression. The results showed that EZH2 was up-regulated and miR-340 was down-regulated in both Hep-2 cells and LSCC tissues. Molecularly, our results confirmed that miR-340 directly targeted EZH2 gene and inhibited EZH2 expression. MTT assay and BrdU assay showed that miR-340 transfection reduced the cell proliferation ability of Hep-2 cells. The transwell assay indicated that the invasion and migration ability of Hep-2 cells was dramatically inhibited by miR-340 transfection. In addition, miR-340 transfection induced cell apoptosis with concomitant enhancement of Bax, increase of Caspase-3 expression and activity, and reduction of Bcl-2 expression in Hep-2 cells. Both miR-340 transfection and EZH2 knockdown induced p27 expression and suppressed PI3K/Akt activation in Hep-2 cells. Strikingly, EZH2 knockdown reduced cell proliferation, and EZH2 overexpression significantly rescued the miR-340-mediated suppressive effect on cell proliferation. Moreover, miR-340 could obviously induce the inhibition of Hep-2 cell-derived tumor growth and EZH2/p27 expression ratio in vivo. Taken together, these data suggest that miR-340 impedes LSCC progression by targeting EZH2 with the possible mechanism to enhance the expression of anti-oncogene p27 and suppress PI3K/Akt activation, providing a novel target and a potential therapeutic pathway against LSCC.