Local anesthetic delivery systems for the management of postoperative pain.

Postoperative pain (POP) is a major clinical challenge. Local anesthetics (LAs), including amide-type LAs, ester-type LAs, and other potential ion-channel blockers, are emerging as drugs for POP management because of their effectiveness and affordability. However, LAs typically exhibit short durations of action and prolonging the duration by increasing their dosage or concentration may increase the risk of motor block or systemic local anesthetic toxicity. In addition, techniques using LAs, such as intrathecal infusion, require professional operation and are prone to catheter displacement, dislodgement, infection, and nerve damage. With the development of materials science and nanotechnology, various LAs delivery systems have been developed to compensate for these disadvantages. Numerous delivery systems have been designed to continuously release a safe dose in a single administration to ensure minimal systemic toxicity and prolong pain relief. LAs delivery systems can also be designed to control the duration and intensity of analgesia according to changes in the external trigger conditions, achieve on-demand analgesia, and significantly improve pain relief and patient satisfaction. In this review, we summarize POP pathways, animal models and methods for POP testing, and highlight LAs delivery systems for POP management. STATEMENT OF SIGNIFICANCE: Postoperative pain (POP) is a major clinical challenge. Local anesthetics (LAs) are emerging as drugs for POP management because of their effectiveness and affordability. However, they exhibit short durations and toxicity. Various LAs delivery systems have been developed to compensate for these disadvantages. They have been designed to continuously release a safe dose in a single administration to ensure minimal toxicity and prolong pain relief. LAs delivery systems can also be designed to control the duration and intensity of analgesia to achieve on-demand analgesia, and significantly improve pain relief and patient satisfaction. In this paper, we summarize POP pathways, animal models, and methods for POP testing and highlight LAs delivery systems for POP management.

The antagonistic effect of FTO on METTL14 promotes AKT3 m6A demethylation and the progression of esophageal cancer.

BACKGROUND: As the most abundant modification in eukaryotic messenger RNAs (mRNAs), N6-methyladenosine (m6A) plays vital roles in many biological processes. METHODS: Methylated RNA immunoprecipitation sequencing (MeRIP-seq) and transcriptomic RNA sequencing (RNA-seq) were used to screen for m6A targets in esophageal cancer cells and patients. The role of m6A RNA methylase in esophageal cancer was also analyzed using bioinformatics. In vitro and in vivo experiments were used to analyze gene expression and function. CCK-8, colony formation, cell apoptosis and immunofluorescence staining assays were performed to evaluate the proliferation, migration and invasion of esophageal cancer cells, respectively. Western blot analysis, RNA stability, RIP and luciferase reporter assays were performed to elucidate the underlying mechanism involved. RESULTS: We found that the m6A demethylase FTO was significantly upregulated in esophageal cancer cell lines and patient tissues. In vivo and in vitro assays demonstrated that FTO was involved in the proliferation and apoptosis of esophageal cancer cells. Moreover, we found that the m6A methyltransferase METTL14 negatively regulates FTO function in esophageal cancer progression. FTO alone is not related to the prognosis of esophageal cancer, and its function is antagonized by METTL14. By using transcriptome-wide m6A-seq and RNA-seq assays, we revealed that AKT3 is a downstream target of FTO and acts in concert to regulate the tumorigenesis and metastasis of esophageal cancer. Taken together, these findings provide insight into m6A-mediated tumorigenesis in esophageal cancer and could lead to the design of new therapeutic strategies.

HIF-1A as a prognostic biomarker related to invasion, migration and immunosuppression of cervical cancer.

Background: The incidence of cervical cancer ranks second among malignant tumors in women, exerting a significant impact on their quality of life and overall well-being. The hypoxic microenvironment plays a pivotal role in the initiation and progression of tumorigenesis. The present study aims to investigate the fundamental genes and pathways associated with the hypoxia-inducible factor (HIF-1A) in cervical cancer, aiming to identify potential downstream targets for diagnostic and therapeutic purposes. Methods: We obtained dataset GSE63514 from the Comprehensive Gene Expression Database (GEO). The dataset comprised of 24 patients in the normal group and 28 patients in the tumor group. Gene set difference analysis (GSVA) and gene set enrichment analysis (GSEA) were used to identify the genes related to HIF-1A expression and the specific signaling pathways involved.The association between HIF-1A and tumor immune infiltration was examined in the TCGA dataset. The WGCAN network was constructed to identify key genes within the blue module, and subsequent gene ontology (GO) function and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were conducted to determine the pathways and functional annotations associated with HIF-1A. The protein interaction network of the HIF-1A gene was obtained from the STRING database and visualized using Cytoscape in the meantime.The function of HIF-1A and its related gene expression were verified in vivo. Results: HIF-1A was a risk factor in both univariate and multivariate Cox regression analysis of cervical cancer patients. A total of 344 genes significantly correlated with the expression of HIF-1A were identified through correlation analysis, and the genes exhibiting the strongest correlation were obtained. The major signaling pathways involved in HIF-1A encompass TNF-α/NF-κB, PI3K/AKT/MTOR, TGF-ß, JAK-STAT, and various other signaling cascades. Reinforced by qRT-PCR, we identified Integrin beta-1 (ITGB1), C-C motif chemokine ligand 2 (CCL2), striatin 3 (STRN3), and endothelin-1 (EDN1) as pivotal downstream genes influenced by HIF-1A. HIF-1A is associated with immune infiltration of natural killer (NK) cells, mast cells, CD4+T cells, M0 macrophages, neutrophils, follicular helper T cells, CD8+T cells, and regulatory T cells (Treg). HIF-1A is associated with sensitivity to chemotherapy drugs. The identification of the HIF-1A pathway and its function primarily focuses on cytoplasmic translation, aerobic respiration, cellular respiration, oxidative phosphorylation, thermogenesis, among others. The results of in vivo experiments have confirmed that HIF-1A plays a crucial role in promoting the migration and invasion of cervical cancer cells. Moreover, the overexpression of HIF-1A led to an upregulation in the expressions of ITGB1, CCL2, STRN3, and EDN1. Conclusions: The role of HIF-1A in cervical cancer was determined through a combination of bioinformatics analysis and experimental validation. The genes potentially implicated in the tumorigenesis mechanism of HIF-1A were identified. These findings has the potential to enhance our comprehension of the progression of cervical cancer and offer promising therapeutic targets for its clinical management.

Efficacy and safety of remimazolam for procedural sedation during ultrasound-guided transversus abdominis plane block and rectus sheath block in patients undergoing abdominal tumor surgery: a single-center randomized controlled trial.

BACKGROUND: To explore the efficacy and safety of remimazolam for procedural sedation during ultrasound-guided nerve block administration in patients undergoing abdominal tumor surgery, in order to improve and optimize remimazolam use in procedural sedation and clinical anesthesia. METHODS: The enrolled patients were randomly divided into three groups: 50 patients in the remimazolam group (R group), 50 patients in the dexmedetomidine group (D group), and 50 patients in the midazolam group (M group). Before administering an ultrasound-guided nerve block, all patients received sufentanil AND remimazolam or midazolam or dexmedetomidine. Remimazolam 5 mg was administered intravenously in group R, dexmedetomidine 0.6 µg/kg was administered intravenously in group D, and midazolam 0.025 mg/kg was administered intravenously in group M. Sedation was evaluated by the Modified Observer's Assessment of Alertness and Sedation scale.When the Modified Observer's Alertness/Sedation (MOAA/S) score was ≤ 2, block operation was started. If the target sedation level was not reached, rescue sedatives of remimazolam 2.5 mg may be intravenously given in group R, dexmedetomidine 0.4 µg/kg be intravenously given in group D, 0.01 mg/kg midazolam may be intravenously given in Group M. Hemodynamic indicators (systolic and diastolic blood pressure, heart rate), pulse oxygen saturation, depth of anesthesia (Narcotrend), MOAA/S,and the incidences of hypoxemia, injection pain, bradycardia and requirement for rescue sedatives were monitored and recorded. RESULTS: Compared with the control groups (midazolam and dexmedetomidine groups), the Narcotrend index and MOAA/S decreased more in the remimazolam group (P < 0.01). Compared with the control groups, the incidence of hypoxemia and injection pain was slightly higher in the remimazolam group, but the difference was not statistically significant (P > 0.05). Compared with the dexmedetomidine group, the incidence of bradycardia was significantly lower in the remimazolam group. CONCLUSION: Remimazolam can be used safely for procedural sedation during ultrasound-guided nerve block administration in patients undergoing abdominal tumor surgery. The sedation effect is better than that with either midazolam or dexmedetomidine, and sedation can be achieved quickly without obvious hemodynamic fluctuations. Remimazolam is associated with better heart rate stability, and slightly higher incidences of hypoxemia and injection pain than are midazolam and dexmedetomidine (no statistically significant difference). The higher incidence of hypoxemia with remimazolam may be related to enhanced sufentanil opioid analgesia, and the mechanism of injection pain with remimazolam must be studied further and clarified. TRIAL REGISTRATION: This study was approved by the Ethics Committee of Anhui Provincial Cancer Hospital (Ethical Review 2021, No. 23) and registered at https://www.chictr.org.cn  (ChiCTR2000035388). The pre-registration time of this experiment is 09/08/2020, due to ethical committee of the hospital met irregularly,the ethical approval time is 21/06/2021. The recruitment of patients began after the ethical approval (21/06/2021) and registration update (06/07/2021).The study protocol followed the CONSORT guidelines. The study protocol was performed in the relevant guidelines.

METTL3/m6A/IFIT2 regulates proliferation, invasion and immunity in esophageal squamous cell carcinoma.

Epigenetic regulation plays a critical role in the development, progression, and treatment of tumors. The most common chemical modification of mRNA, called m6A, is essential for controlling mRNA stability, splicing, and translation. Methyltransferase-like 3 (METTL3) is an important m6A methyltransferase. The mechanism of action of METTL3 in esophageal squamous cell carcinoma (ESCC) remains unclear. In this investigation, we sought to clarify the function and clinical importance of METTL3 in ESCC and investigate its underlying mechanisms. We discovered that METTL3 has a significant proliferative effect in ESCC cells by using lentiviral construction of stable cell lines overexpressing METTL3 (METTL3-OE) and knocking down METTL3 (sh-METTL3). To create a xenograft tumor model, we inoculated KYSE510 cells subcutaneously into BALB/c nude mice and discovered that sh-METTL3 inhibited the tumorigenicity of esophageal cancer KYSE510 cells in the nude mouse tumor model. MeRIP-seq and RNA-seq analysis revealed IFIT2 to be a METTL3 target gene. The findings revealed that METTL3 regulates IFIT2 and thus influences malignant biological behaviors such as proliferation, migration, and invasion of ESCC, as well as the immune microenvironment of tumors.

FTO mediated ERBB2 demethylation promotes tumor progression in esophageal squamous cell carcinoma cells.

N6-methyladenosine (m6A) is the most prevalent and internal modification that occurs in the messenger RNAs of eukaryotes. However, knowledge of the impact of these modifications on gene expression regulation remains limited. By using the in vitro MeRIP-seq and RNA-seq assays, we discovered that the mRNA demethylase FTO was significantly up-regulated in esophageal squamous cell carcinoma (ESCC) tissues and cells. Knockdown of FTO drastically suppressed the proliferation, migration, and invasion of ESCC cells. Furthermore, by using transcriptome-wide m6A-seq and RNA-seq assays, we identified ERBB2 is the target of FTO, which acts in concert in ESCC tumorigenesis and metastasis. Moreover, loss and gain functional studies suggested that the m6A reader YTHDF1 stabilizes ERBB2 mRNA via decoding the m6A modification. All these results uncovered a new signaling cascade, including FTO, YTHDF1, and ERBB2, which finely regulates the ESCC progression.

Establishment of predicting equation for individual sufentanil dosage postoperatively based on gene polymorphisms.

BACKGROUND: Postoperative analgesia is widely used for patients undergoing major surgeries. Individual differences in genetic polymorphisms may be obstructive factors for accurately anesthetics using. However, the equation for predicting sufentanil dosage postoperatively based on genetic design has been established yet. Our aim was to establish sufentanil dosage postoperatively prediction equation based on patients' genetic polymorphisms. METHODS: One hundred forty patients with total gastrectomy and radical resection of pulmonary carcinoma were included. To establish sufentanil dosage postoperatively for patients with gastric cancer, we collected patients' basic information and CYP3A4*1G, COMTVal158Met, OPRM1A118G, and ABCB1C3435T gene sequencing results. To verify this equation, we put patients' with lung cancer surgeries information into it. RESULTS: The sufentanil dosage prediction equation postoperatively was y = 4.104 - 0.222 × (gender) + 0.021 × (OPRM1A118G) + 0.249 × (ABCB1C3435T). Patients' with lung cancer surgeries information were substituted into it. The results showed no significant differences between predicted and actual sufentanil dosage (p > 0.05). CONCLUSION: We established the prediction equation for individual sufentanil dosage postoperatively based on gene polymorphisms. The results showed this prediction equation was valid, which might be used for different types of surgeries. We established an equation for individual dosage of sufentanil for postoperative analgesia based on gene polymorphisms. The results show that the prediction equation is valid, the information might be used for different types of postoperative analgesia, and the painful patients will have great potential safe and personalized pain control after analgesic therapy. It might also have potential as a clinical tool.

The significance of glycolysis in tumor progression and its relationship with the tumor microenvironment.

It is well known that tumor cells rely mainly on aerobic glycolysis for energy production even in the presence of oxygen, and glycolysis is a known modulator of tumorigenesis and tumor development. The tumor microenvironment (TME) is composed of tumor cells, various immune cells, cytokines, and extracellular matrix, among other factors, and is a complex niche supporting the survival and development of tumor cells and through which they interact and co-evolve with other tumor cells. In recent years, there has been a renewed interest in glycolysis and the TME. Many studies have found that glycolysis promotes tumor growth, metastasis, and chemoresistance, as well as inhibiting the apoptosis of tumor cells. In addition, lactic acid, a metabolite of glycolysis, can also accumulate in the TME, leading to reduced extracellular pH and immunosuppression, and affecting the TME. This review discusses the significance of glycolysis in tumor development, its association with the TME, and potential glycolysis-targeted therapies, to provide new ideas for the clinical treatment of tumors.

A New Functional Gene, Zinc Finger Protein 485 (ZNF485), is Involved in Bladder Cancer Proliferation.

BACKGROUND: Bladder cancer is the second most common urological cancer worldwide, with low early diagnosis and high mortality. The limited progress in diagnostics and treatment greatly impedes the survival of bladder cancer patients. OBJECTIVE: Potential therapeutic biomarkers are urgently needed for future clinical treatment. METHODS: We analyzed the sequencing data and corresponding clinicopathological features and survival information of bladder cancer patients in the TCGA database and identified a new zinc finger protein 485 gene, termed ZNF485, which is highly expressed in the tissues of bladder cancer patients and was verified in cells, animal models and tissue microarrays. RESULTS: We found that inhibition of ZNF485 in the bladder cancer cell lines T24 and 5637 obviously inhibited proliferation and promoted the apoptosis of cancer cells. Furthermore, wound healing and invasion assays showed that downregulation of ZNF485 significantly decreased the mobility and invasion of T24 and 5637 cells. In addition, ZNF485-shRNA transfection obviously inhibited tumor growth in nude mice. Immunohistochemical results of clinical samples showed that the expression level of ZNF485 protein in cancer tissues was higher than that in adjacent tissues. Mechanistic analysis identified possible downstream target genes. CONCLUSIONS: Taken together, the results provide evidence that ZNF485 is involved in bladder cancer proliferation and might be a potential therapeutic biomarker for the treatment of this disease.

LAMTOR5-AS1 regulates chemotherapy-induced oxidative stress by controlling the expression level and transcriptional activity of NRF2 in osteosarcoma cells.

Long-noncoding RNAs (lncRNAs) play roles in regulating cellular functions. High-throughput sequencing analysis identified a new lncRNA, termed LAMTOR5-AS1, the expression of which was much higher in the chemosensitive osteosarcoma (OS) cell line G-292 than in the chemoresistant cell line SJSA-1. Further investigations revealed that LAMTOR5-AS1 significantly inhibits the proliferation and multidrug resistance of OS cells. In vitro assays demonstrated that LAMTOR5-AS1 mediates the interaction between nuclear factor erythroid 2-related factor 2 (NFE2L2, NRF2) and kelch-like ECH-associated protein 1 (KEAP1), which regulate the oxidative stress. Further mechanistic studies revealed that LAMTOR5-AS1 inhibited the ubiquitination degradation pathway of NRF2, resulting in a higher level of NRF2 but a loss of NRF2 transcriptional activity. High level of NRF2 in return upregulated the downstream gene heme oxygenase 1 (HO-1). Moreover, NRF2 controls its own activity by promoting LAMTOR5-AS1 expression, whereas the feedback regulation is weakened in drug-resistant cells due to high antioxidant activity. Overall, we propose that LAMTOR5-AS1 globally regulates chemotherapy-induced cellular oxidative stress by controlling the expression and activity of NRF2.

Long Noncoding RNA DICER1-AS1 Functions in Methylation Regulation on the Multi-Drugresistance of Osteosarcoma Cells via miR-34a-5p and GADD45A.

Osteosarcoma (OS) is a common malignant bone tumor that commonly occurs in children and adolescents. Long noncoding RNAs (lncRNAs) are recognized as a novel class of regulators of gene expression associated with tumorigenesis. However, the effect and mechanism of lncRNAs in OS tumorigenesis and drug resistance have not been characterized. The purpose of the study is to screen potential biomarker and therapeutic target against OS. We compared the lncRNA expression profiles between OS cell lines with different drug resistance levels using RNA-seq analysis and found that lncRNA DICER1-AS1 was significantly differentially expressed in multi-drugresistant OS cells SJSA-1 versus multi-drugsensitive OS cells G-292. Bisulfite Sequencing PCR (BSP) assay was performed to analyze the differential methylation status of the promoter region of DICER1-AS1 in four OS cells. Subsequently, in vitro gain- and loss-of-function experiments demonstrated the roles of DICER1-AS1 and miR-34a-5p in the multi-drugresistance of OS cells. The main findings is that DICER1-AS1 directly binds to miR-34a-5p, and their expression has a negative correlation with each other. The hypermethylation of the promoter region of DICER1-AS1 silenced its expression in the drugresistant cells SJSA-1 and MNNG/HOS. Moreover, we found that growth arrest and DNA damage-inducible alpha (GADD45A) participates in the DICER1-AS1/miR-34a-5p-regulated drug resistance of OS cells, probably via the cell cycle/pRb-E2F pathway. Our results revealed DICER1-AS1/miR-34a-5p-regulated drug resistance of OS cells, a new lncRNA-regulated network in OS tumorigenesis, suggested that DICER1-AS1 can be considered as a potential biomarker and therapeutic target against OS cells.

The DNA methylation-regulated MCTP1 activates the drug-resistance of esophageal cancer cells.

Accumulating studies have demonstrated that drug-resistance remains a great obstacle for the effective treatment of cancers. Esophageal cancer is still one of the most common cancers worldwide, which also suffers from the drug-resistance during clinical treatment. Here we performed drug-resistance profiling assays and identified several drug-resistant and drug-sensitive esophageal cancer cell lines. The following methylation sequencing showed that the MCTP1 gene is hypermethylated in the drug-resistant esophageal cancer cells. As a result, the expression of MCTP1 is down-regulated in the drug-resistant esophageal cancer cells. Down-regulation of MCTP1 also affects the migration and apoptosis of esophageal cancer cells, as revealed by the wound-healing and apoptosis assays. Further investigations proposed two signaling pathways that might involve in the MCTP1-mediated drug-resistance of esophageal cancer cells. All these results suggested that MCTP1 activates the drug-resistance of esophageal cancer cells, which has implications for further design of new biomarker of esophageal cancer treatment.

Association between CD24 Ala/Val polymorphism and multiple sclerosis risk: A meta analysis.

BACKGROUND: The aim of this study was to explore the association between CD24 Ala/Val polymorphism and susceptibility of multiple sclerosis (MS). METHODS: A comprehensive literature search for relevant studies was performed on google scholar, PubMed, Web of science, Embase, the Chinese National Knowledge Infrastructure and the Chinese Biology Medicine. This meta-analysis was conducted using the STATA 11.0 software and the pooled odds ratio with 95% confidence interval was calculated. RESULTS: Seven case-control studies were included in this meta-analysis. The results showed significant association between CD24 Ala/Val polymorphism and susceptibility to MS. Stratified analysis by areas also showed significant association in Asians. However, no association was found in Europeans. CONCLUSION: This study suggested that the CD24 Val allele was associated with an increased risk of MS and larger-scale studies of populations are needed to explore the role of CD24 Ala/Val polymorphism during the pathogenesis of MS.

Ribosomal protein small subunit 15A (RPS15A) inhibits the apoptosis of breast cancer MDA-MB-231 cells via upregulating phosphorylated ERK1/2, Bad, and Chk1.

AIM: To detect the expression and identify the role of Ribosomal protein S15A (RPS15A) in human breast cancer (BC). METHODS: Immunohistochemistry (IHC) was carried out for detecting the levels of RPS15A protein. Quantitative PCR was used to evaluate the mRNA level of RPS15A in one normal breast and three BC cell lines. Lentivirus-mediated shRNA targeting RPS15A was designed to investigate the impact of silencing RPS15A in MDA-MB-231 cell. RESULTS: Higher RPS15A expression was detected in tumor tissues than in para-cancer tissues, and higher RPS15A expression was related to larger tumor size and higher TNM stage. Also, RPS15A mRNA expression in all three BC cell lines was higher than that in normal breast cell (all P < .005). Further, RPS15A knockdown significantly suppressed MDA-MB-231 cell proliferation and induced apoptosis. Moreover, RPS15A knockdown increased the caspase-3/-7 activity, and suppressed the phosphorylated levels of ERK1/2, Bad, and Chk1 (all P < .01). CONCLUSION: RPS15A inhibits apoptosis via upregulating phosphorylated ERK1/2, Bad, and Chk1 in MDA-MB-231 cell line.

Effect of dexmedetomidine on postoperative cognitive dysfunction and inflammation in patients after general anaesthesia: A PRISMA-compliant systematic review and meta-analysis.

BACKGROUND: Neuroprotective effects of dexmedetomidine are reported in preclinical and clinical studies but evidence regarding the postoperative neurocognitive function is still unclear. This study performed a meta-analysis on outcomes of studies which examined neurocognitive performance and inflammatory factors to investigate the effects of dexmedetomidine on postoperative cognitive dysfunction (POCD) and inflammation in patients after general anaesthesia. METHODS: Literatures were searched in several electronic databases and studies were selected by following precise inclusion criteria. We searched PubMed, EMBASE, the Cochrane Library, China Academic Journals full-text database (CNKI), and Google Scholar to find randomized controlled trials (RCTs) of the influence of dexmedetomidine on POCD and inflammation in patients who had undergone general anaesthesia. Two researchers independently screened the literature, extracted data, and evaluated quality of methodology against inclusion and exclusion criteria. Meta-analyses of pooled ORs of POCD incidences and mean differences in neurocognitive assessment scores and inflammation levels were carried out and subgroup analyses were performed. Stata 12.0 was used to conduct our meta-analysis. RESULTS: Twenty-six RCTs were included. Compared with controls, perioperative dexmedetomidine treatment significantly reduced the incidence of POCD (pooled ORs = 0.59, 95% confidence interval (CI) 0.45-2.95) and improved Mini-Mental State Examination (MMSE) score (standardized mean difference (SMD) = 1.74, 95% CI 0.43-3.05) on the first postoperative day. Furthermore, perioperative dexmedetomidine treatment significantly decreased IL-6 (SMD = -1.31, 95% CI -1.87-0.75, P < .001) and TNF-α (SMD = -2.14, 95% CI -3.14-1.14, P < .001) compared to saline/comparators treatment. In the stratified analysis by surgical type, age, type of control, and study region, the differences were also significant between dexmedetomidine- and saline-treated patients. CONCLUSION: Perioperative dexmedetomidine treatment is associated with significantly reduced incidence of POCD and inflammation and better neurocognitive function postoperatively in comparison with both saline controls and comparator anaesthetics.

miR-193a-3p Promotes Radio-Resistance of Nasopharyngeal Cancer Cells by Targeting SRSF2 Gene and Hypoxia Signaling Pathway.

BACKGROUND Radio-resistance is an important barrier in nasopharyngeal carcinoma treatment. MicroRNAs are gene expression core regulators in various biological procedures containing cancer radio-resistance. Nevertheless, the clinical association between nasopharyngeal carcinoma and miR-193a-3p/SRSF2 remains unclear. MATERIAL AND METHODS We examined the miR-193a-3p level in radio-sensitive CNE-2 and radio-resistant CNE-1 NPC cell lines, and, based on a literature review, predicted SRSF2 to be the target gene of miR-193a-3p. We explored the expression of SRSF2 at protein and mRNA levels by transfecting either miR-193a-3p-mimic or antagomiR. Finally, we performed signaling pathway analysis to assess the possible role of miR-193a-3p/SRSF2 in signaling pathways. RESULTS miR-193a-3p promotes NPC radio-resistance, and the SRSF2 gene is the direct target for miR-193a-3p in NPC, and thus is negatively correlated with NPC radio-resistance. The hypoxia signaling pathway activity is strongly affected, and it is possible to use the downstream activity of the SRSF2 gene to show the effect of miR-193a-3p on radio-resistance in NPC cells. CONCLUSIONS miR-193a-3p mediates promotion of NPC radio-resistance.