Transposition of the lingual thyroid gland to the submandibular region through a submandibular approach: A case report.

BACKGROUND: Ectopic thyroid at the base of the tongue is a rare congenital condition, and it is even rarer to have clinical symptoms and require surgical intervention. This disease is easily misdiagnosed preoperatively. This article reports the diagnosis, surgical treatment, and follow-up of a case of lingual thyroid. CASE SUMMARY: The patient was a 54-year-old woman who presented with laryngeal foreign body sensation and dysphagia for 20 d. The lingual thyroid was considered for general examination, and surgery was performed to transpose the lingual thyroid to the right submaxillary region. Pathological analysis confirmed thyroid tissue. The patient experienced complete remission after surgery, but developed hypothyroidism and required thyroid hormone replacement therapy, and her thyroid function gradually recovered over time. CONCLUSION: We report a rare case of lingual thyroid with marked laryngeal foreign body sensation and dysphagia. Symptoms were completely relieved by transposition surgery but postoperative hypothyroidism developed.

Compound collagen peptide powder improves skin photoaging by reducing oxidative stress and activating TGF-ß1/Smad pathway.

Fish collagen peptide (FCP) has been extensively investigated as a natural product that can combat photoaging; however, its efficacy is limited by its singular composition. Compound collagen peptide powder (CCPP) is a novel functional food formulation that exhibits photoprotective properties and comprises FCP and a blend of natural botanical ingredients. The objective of this study was to investigate the efficacy of CCPP and its molecular mechanism. CCPP had a low molecular weight, facilitating its efficient absorption, and was abundant in amino acids, total polyphenols, and total flavonoids. The results of in vivo studies demonstrated that CCPP exhibited significant efficacy in reducing skin wrinkles, enhancing the contents of water and oil in the skin, and ameliorating histopathological alterations in mice. The results of in vitro studies demonstrated that CCPP effectively mitigated photoaging in human skin fibroblasts by attenuating oxidative stress and promoting extracellular matrix (ECM) synthesis. Moreover, we clearly demonstrated that the TGF ß1/Smad pathway was involved in the promotion of ECM synthesis and cell proliferation by CCPP in human skin fibroblasts. These findings suggest that, compared with single collagen, CCPP has a more comprehensive range of antiphotoaging properties.

TRIM29 modulates proteins involved in PTEN/AKT/mTOR and JAK2/STAT3 signaling pathway and suppresses the progression of hepatocellular carcinoma.

Tripartite motif-containing 29 (TRIM29), also known as the ataxia telangiectasia group D-complementing (ATDC) gene, has been reported to play an oncogenic or tumor suppressive role in developing different tumors. So far, its expression and biological functions in hepatocellular carcinoma (HCC) remain unclear. We investigated TRIM29 expression pattern in human HCC samples using quantitative RT-PCR and immunohistochemistry. Relationships between TRIM29 expression level, clinical prognostic indicators, overall survival (OS), and disease-free survival (DFS) were evaluated by Kaplan-Meier analysis and Cox proportional hazards model. A series of in vitro experiments and a xenograft tumor model were conducted to detect the functions of TRIM29 in HCC cells. RNA sequencing, western blotting, and immunochemical staining were performed to assess the molecular regulation of TRIM29 in HCC. We found that the mRNA and protein levels of TRIM29 were significantly reduced in HCC samples, compared with adjacent noncancerous tissues, and were negatively correlated with poor differentiation of HCC tissues. Survival analysis confirmed that lower TRIM29 expression significantly correlated with shorter OS and DFS of HCC patients. TRIM29 overexpression remarkably inhibited cell proliferation, migration, and EMT in HCC cells, whereas knockdown of TRIM29 reversed these effects. Moreover, deactivation of the PTEN/AKT/mTOR and JAK2/STAT3 pathways might be involved in the tumor suppressive role of TRIM29 in HCC. Our findings indicate that TRIM29 in HCC exerts its tumor suppressive effects through inhibition of the PTEN/AKT/mTOR and JAK2/STAT3 signaling pathways and may be used as a potential biomarker for survival in patients with HCC.

Pien Tze Huang alleviates Concanavalin A-induced autoimmune hepatitis by regulating intestinal microbiota and memory regulatory T cells.

BACKGROUND: Traditional Chinese medicine has used the drug Pien Tze Huang (PTH), a classic prescription, to treat autoimmune hepatitis (AIH). However, the precise mode of action is still unknown. AIM: To investigate the mechanism of PTH in an AIH mouse model by determining the changes in gut microbiota structure and memory regulatory T (mTreg) cells functional levels. METHODS: Following induction of the AIH mouse model induced by Concanavalin A (Con A), prophylactic administration of PTH was given for 10 d. The levels of mTreg cells were measured by flow cytometry, and intestinal microbiota was analyzed by 16S rRNA analysis, while western blotting was used to identify activation of the toll-like receptor (TLR)2, TLR4/nuclear factor-κB (NF-κB), and CXCL16/CXCR6 signaling pathways. RESULTS: In the liver of mice with AIH, PTH relieved the pathological damage and reduced the numbers of T helper type 17 cells and interferon-γ, tumor necrosis factor-alpha, interleukin (IL)-1ß, IL-2, IL-6, and IL-21 expression. Simultaneously, PTH stimulated the abundance of helpful bacteria, promoted activation of the TLR2 signal, which may enhance Treg/mTreg cells quantity to produce IL-10, and suppressed activation of the TLR4/NF-κB and CXCL16/CXCR6 signaling pathways. CONCLUSION: PTH regulates intestinal microbiota balance and restores mTreg cells to alleviate experimental AIH, which is closely related to the TLR/CXCL16/CXCR6/NF-κB signaling pathway.

PD1hi CD200hi CD4+ exhausted T cell increase immunotherapy resistance and tumour progression by promoting epithelial-mesenchymal transition in bladder cancer.

BACKGROUND: Bladder cancer (BLCA) is one of the most diagnosed cancers in humans worldwide. Recently, immunotherapy has become a main treatment option for BC. However, most BLCA patients do not respond to immune checkpoint inhibitors or relapse after immunotherapy. Therefore, it is very important to identify novel biomarkers for the prediction of immunotherapy response in B patients. METHODS: Pancancer single-cell RNA sequencing (scRNA-seq) data were used to identify the clusters of CD4+ T cells in the tumour microenvironment (TME). The clinical significance of key CD4+ T-cell clusters was evaluated based on the survival data of two independent immunotherapy bladder cancer (BLCA) cohorts. We also investigated the function of key clusters of CD4+ T cell in the TME of BC cells in vitro. RESULTS: This study identified two novel exhausted CD4+ T-cell subpopulations with the expression of PD1hi CD200hi or PD1hi CD200low in BC patients. Moreover, BLCA patients with a high level of PD1hi CD200hi CD4+ exhausted T cell showed immunotherapy resistance. Cell function analysis demonstrated that PD1hi CD200hi CD4+ exhausted T cell can promote epithelial-mesenchymal transition (EMT) and angiogenesis in BLCA cells. In addition, PD1hi CD200hi CD4+ exhausted T cells were shown to communicate with malignant BLCA cells through the GAS6-AXL axis. Finally, we also found that GAS6 expression is upregulated in B cells by METTL3-mediated m6A modification. CONCLUSIONS: PD1hi CD200hi CD4+ exhausted T cell may serve as a novel biomarker for poor prognosis and immunotherapy resistance in B. Targeted inhibitors of PD1hi CD200hi CD4+ exhausted T cells may help improve the efficacy of immunotherapy.

High density and proximity of CD8+ T cells to tumor cells are correlated with better response to nivolumab treatment in metastatic pleural mesothelioma.

BACKGROUND: The efficacy of immune checkpoint inhibitors (ICIs) in pleural mesothelioma has recently been established. The response to ICIs can be predicted by quantitative analysis of cells and their spatial distribution in the tumor microenvironment (TME). However, the detailed composition of the TME in pleural mesothelioma has not been reported. We evaluated the association between the TME and response to ICIs in this cancer. METHODS: A retrospective analysis of 22 pleural mesothelioma patients treated with nivolumab in different centers was performed using surgical specimens. Four patients had a partial response to nivolumab (response group) and 18 patients had stable or progressive disease (nonresponse group). The number of CD4, CD8, FoxP3, CK, and PD-L1 positive cells, cell density, and cell-to-cell distance were analyzed by multiplex immunofluorescence. RESULTS: PD-L1 expression did not differ significantly between the response and nonresponse groups. The density of total T cells and of CD8+ T cells was significantly higher in the response than in the nonresponse group. CD8+ T cells were more clustered and located closer to tumor cells, whereas regulatory T cells were located further from tumor cells in the response than in the nonresponse group. CONCLUSIONS: High density and spatial proximity of CD8+ T cells to tumor cells were associated with better response to nivolumab, whereas the proximity of regulatory T cells to tumor cells was associated with worse response, suggesting that the distinct landscape of the TME could be a potential predictor of ICI efficacy in pleural mesothelioma.

Ezetimibe Induces Paraptosis through Niemann-Pick C1-like 1 Inhibition of Mammalian-Target-of-Rapamycin Signaling in Hepatocellular Carcinoma Cells.

Currently, hepatocellular carcinoma (HCC) is characterized by its unfavorable prognosis and resistance to conventional chemotherapy and radiotherapy. Drug repositioning, an approach aimed at identifying novel therapeutic applications for existing drugs, presents a cost-effective strategy for developing new anticancer agents. We explored the anticancer properties of Ezetimibe, a widely used oral lipid-lowering drug, in the context of HCC. Our findings demonstrate that Ezetimibe effectively suppresses HCC cell proliferation through paraptosis, an apoptotic-independent cell death pathway. The examination of HCC cells lines treated with Ezetimibe using light microscopy and transmission electron microscopy (TEM) showed cytoplasmic vacuolation in the perinuclear region. Notably, the nuclear membrane remained intact in both Ezetimibe-treated and untreated HCC cell lines. Probe staining assays confirmed that the cytoplasmic vacuoles originated from dilated endoplasmic reticulum (ER) compartments rather than mitochondria. Furthermore, a dose-dependent accumulation of reactive oxygen species (ROS) was observed in Ezetimibe-treated HCC cell lines. Co-treatment with the general antioxidant NAC attenuated vacuolation and improved cell viability in Ezetimibe-treated HCC cells. Moreover, Ezetimibe induced paraptosis through proteasome activity inhibition and initiation of the unfolded protein response (UPR) in HCC cell lines. In our in vivo experiment, Ezetimibe significantly impeded the growth of HCC tumors. Furthermore, when combined with Sorafenib, Ezetimibe exhibited a synergistic antitumor effect on HCC cell lines. Mechanistically, Ezetimibe induced paraptosis by targeting NPC1L1 to inhibit the PI3K/AKT/mTOR signaling pathway. In conclusion, our study highlights the potential of Ezetimibe as an anticancer agent by triggering paraptosis in HCC cells.

Self-Expandable Metal Stent in the Management of Malignant Airway Disorders.

Background: Self-expanding metallic stent (SEMS) is a palliative therapy for patients with malignant central airway obstruction (CAO) or tracheoesophageal fistula (TEF). Despite this, many patients experience death shortly after SEMS placement. Aims: We aimed to investigate the effect of SEMS on the palliative treatment between malignant CAO and malignant TEF patients and investigate the associated prognostic factors of the 3-month survival. Methods: We performed a single-center, retrospective study of malignant CAO or TEF patients receiving SEMS placement. Clinical data were collected using the standardized data abstraction forms. Data were analyzed using SPSS 22.0. A two-sided P-value <0.05 was statistically significant. Results: 106 malignant patients (82 CAO and 24 TEF) receiving SEMS placement were included. The body mass index (BMI), hemoglobin levels, and albumin levels in the malignant TEF group were lower than in the malignant CAO group (all P < 0.05). The procalcitonin levels, C-reactive protein levels, and the proportion of inflammatory lesions were higher in the malignant TEF group than in the malignant CAO group (all P < 0.05). The proportion of symptomatic improvement after the SEMS placement was 97.6% in the malignant CAO group, whereas 50.0% in the malignant TEF group, with a significant difference (P = 0.000). Three months after SEMS placement, the survival rate at was 67.0%, significantly lower in the malignant TEF group than in the malignant CAO group (45.8% vs. 73.2%, P = 0.013). Multivariate analysis revealed that BMI [odds ratio (OR) = 1.841, 95% certificated interval (CI) (1.155-2.935), P = 0.010] and neutrophil percentage [OR = 0.936, 95% CI (0.883-0.993), P = 0.027] were the independent risk factors for patients who survived three months after SEMS placement. Conclusions: We observed symptom improvement in malignant CAO and TEF patients after SEMS placement. The survival rate in malignant TEF patients after SEMS placement was low, probably due to aspiration pneumonitis and malnutrition. Therefore, we recommend more aggressive treatment modalities in patients with malignant TEF, such as strong antibiotics, nutrition support, and strategic ventilation. More studies are needed to investigate the prognostic factors in patients with malignant airway disorders receiving SEMS placement.

A case report of dermatomyositis with the missed diagnosis of non-small cell lung cancer and concurrence of pulmonary tuberculosis.

A 42-year-old man with four months of retrosternal pain and two months of skin rashes and proximal muscle weakness was diagnosed with dermatomyositis (DM) based on muscle enzyme analysis and needle electromyography. Chest computed tomography (CT) showed scattered inflammation nodules in both lungs' upper lobes with negative sputum smear for lung cancer and pulmonary tuberculosis (TB). A good clinical response to oral prednisone was obtained, except for the retrosternal pain in the preceding two months. Urgent CT pulmonary angiography ruled out pulmonary thromboembolism but revealed squamous cell lung cancer with metastases in the sternum and mediastinal lymph nodes. In retrospect, we found osteolytic destruction consistent with sternal metastasis on CT taken at the initial treatment of DM, which was missed by radiologists. Simultaneously, the man was diagnosed with pulmonary TB based on rapid mycobacterial TB detection. This case report indicates the radiologic errors and highlights the importance of a thorough search for underlying lung cancer and pulmonary TB in patients with DM, especially in countries with a high TB burden.

Cancer-secreted exosomal miR-21-5p induces angiogenesis and vascular permeability by targeting KRIT1.

Cancer-secreted exosomes are critical mediators of cancer-host crosstalk. In the present study, we showed the delivery of miR-21-5p from colorectal cancer (CRC) cells to endothelial cells via exosomes increased the amount of miR-21-5p in recipient cells. MiR-21-5p suppressed Krev interaction trapped protein 1 (KRIT1) in recipient HUVECs and subsequently activated ß-catenin signaling pathway and increased their downstream targets VEGFa and Ccnd1, which consequently promoted angiogenesis and vascular permeability in CRC. A strong inverse correlation between miR-21-5p and KRIT1 expression levels was observed in CRC-adjacent vessels. Furthermore, miR-21-5p expression in circulating exosomes was markedly higher in CRC patients than in healthy donors. Thus, our data suggest that exosomal miR-21-5p is involved in angiogenesis and vascular permeability in CRC and may be used as a potential new therapeutic target.

Prognostic Significance of Autophagy-Relevant Gene Markers in Colorectal Cancer.

BACKGROUND: Colorectal cancer (CRC) is a common malignant solid tumor with an extremely low survival rate after relapse. Previous investigations have shown that autophagy possesses a crucial function in tumors. However, there is no consensus on the value of autophagy-associated genes in predicting the prognosis of CRC patients. This work screens autophagy-related markers and signaling pathways that may participate in the development of CRC, and establishes a prognostic model of CRC based on autophagy-associated genes. METHODS: Gene transcripts from the TCGA database and autophagy-associated gene data from the GeneCards database were used to obtain expression levels of autophagy-associated genes, followed by Wilcox tests to screen for autophagy-related differentially expressed genes. Then, 11 key autophagy-associated genes were identified through univariate and multivariate Cox proportional hazard regression analysis and used to establish prognostic models. Additionally, immunohistochemical and CRC cell line data were used to evaluate the results of our three autophagy-associated genes EPHB2, NOL3, and SNAI1 in TCGA. Based on the multivariate Cox analysis, risk scores were calculated and used to classify samples into high-risk and low-risk groups. Kaplan-Meier survival analysis, risk profiling, and independent prognosis analysis were carried out. Receiver operating characteristic analysis was performed to estimate the specificity and sensitivity of the prognostic model. Finally, GSEA, GO, and KEGG analysis were performed to identify the relevant signaling pathways. RESULTS: A total of 301 autophagy-related genes were differentially expressed in CRC. The areas under the 1-year, 3-year, and 5-year receiver operating characteristic curves of the autophagy-based prognostic model for CRC were 0.764, 0.751, and 0.729, respectively. GSEA analysis of the model showed significant enrichment in several tumor-relevant pathways and cellular protective biological processes. The expression of EPHB2, IL-13, MAP2, RPN2, and TRAF5 was correlated with microsatellite instability (MSI), while the expression of IL-13, RPN2, and TRAF5 was related to tumor mutation burden (TMB). GO analysis showed that the 11 target autophagy genes were chiefly enriched in mRNA processing, RNA splicing, and regulation of the mRNA metabolic process. KEGG analysis showed enrichment mainly in spliceosomes. We constructed a prognostic risk assessment model based on 11 autophagy-related genes in CRC. CONCLUSION: A prognostic risk assessment model based on 11 autophagy-associated genes was constructed in CRC. The new model suggests directions and ideas for evaluating prognosis and provides guidance to choose better treatment strategies for CRC.

Emerging functions of PRKDC in the initiation and progression of cancer.

The DNA-dependent protein kinase catalytic subunit (DNA-PKcs) is encoded by the protein kinase, DNA-activated, catalytic polypeptide (PRKDC) gene. DNA-PKcs plays a major role in nonhomologous end joining DNA repair, and it has been identified to be an important factor in tumor progression and metastasis. DNA-PKcs may have opposite effects in diseases, depending on the cell and tissue types. In this review, we discuss its role in various tumors. High levels of DNA-PKcs are directly associated with prognosis, neoplasm recurrence rates, and overall survival. Our results suggest that DNA-PKcs may serve as a therapeutic target for advanced malignancies.

The effect of miRNA and autophagy on colorectal cancer.

Colorectal cancer (CRC) has become a concern because of its high recurrence rate and metastasis rate, low early diagnosis rate and poor therapeutic effect. At present, various studies have shown that autophagy is closely connected with the occurrence and progression of CRC. Autophagy is a highly cytosolic catabolic process involved in lysosomes in biological evolution. Cells degrade proteins and damaged organelles by autophagy to achieve material circulation and maintain cell homeostasis. Moreover, microRNAs are key regulators of autophagy, and their mediated regulation of transcriptional and post-transcriptional levels plays an important role in autophagy in CRC cells. This review focuses on the recent research advances of how autophagy and related microRNAs are involved in affecting occurrence and progression of CRC and provides a new perspective for the study of CRC treatment strategies.

Do environmental concentrations of zinc oxide nanoparticle pose ecotoxicological risk to aquatic fungi associated with leaf litter decomposition?

Ecotoxicological risk of ZnO nanoparticles at environmental levels is a key knowledge gap for predicting how freshwater ecosystems will respond to nanoparticle pollution. A microcosm experiment was conducted to explore the chronic effects of ZnO nanoparticle at environmental concentrations (30, 300, 3000 ng L-1) on aquatic fungi associated with the decomposing process of poplar leaf litter (45 days). ZnO nanoparticles led to 9-33% increases in fungal biomass after acute exposure (5 days), but 33-50% decreases after chronic exposure (45 days), indicating that the hormetic effect of ZnO nanoparticles at the environmental level may occur during acute exposure. Besides, ZnO nanoparticles had negative effects on microbial enzyme activity, especially on day 10, when the activities of N-acetylglucosaminidase, glycine-aminopeptidase, aryl-sulfatase, polyphenol oxidase, and peroxidase were significantly inhibited. After chronic exposure, the fungal community structure was significantly impacted by ZnO nanoparticles at 300 ng L-1 due to the reduced proportion of Anguillospora, which eventually caused a significant decrease in litter decomposition rate. Therefore, ZnO nanoparticles may pose ecotoxicological effects on aquatic fungi even at a very low concentration and eventually negatively affect freshwater functioning.

Emerging roles of circRNA in formation and progression of cancer.

Circular RNAs (circRNAs) are recently discovered as a special novel type of endogenous noncoding RNAs (ncRNAs), which form a covalently closed continuous loop and are highly represented in the eukaryotic transcriptome. Recent research revealed that circRNAs can function as microRNA (miRNA) sponges, regulators of splicing and transcription, as well as interact with RNA-binding proteins (RBPs). In this review, not only the function and mechanism, but also the experimental methods of circRNA are summarized. The summary of the current state of circRNA will help us in the discovery of novel biomarkers, the therapeutic targets and their potential significance in diagnosis and treatment of diseases. CircRNAs might play important roles in cancers especially in hepatocellular carcinoma, gastric carcinoma and colorectal cancer as well as serving as diagnostic or predictive biomarkers of some diseases and providing new treatments of diseases.

MicroRNA-34a suppresses the invasion and migration of colorectal cancer cells by enhancing EGR1 and inhibiting vimentin.

MicroRNAs (miRNAs/miRs) are small non-coding RNAs that serve a post-transcriptional regulatory role in eukaryotes. Previous studies have demonstrated that the expression of miR-34a in colorectal cancer (CRC) tissues is decreased compared with that in normal colorectal tissues. However, the role of miR-34a in the invasion and metastasis of CRC remains unclear. In the present study, the levels of miR-34a expression were measured in various CRC cell lines. The cells were transfected with miR-34a mimics or inhibitors in order to assess the proliferation rate, and the colony forming, invasive and migratory abilities. Furthermore, the protein expression levels of vimentin and early growth response protein 1 (EGR1) were examined by western blot analysis. The results revealed that the expression of miR-34a was low in SW620, RKO, LoVo and Caco-2 cell lines and high in the SW480 and SW1116 cell lines. The migration, invasion and proliferation levels of SW480 cells were facilitated by decreasing the expression of miR-34a. Transient transfection with miR-34a mimics in SW620 cells caused a notable decrease in cell migration, invasion and proliferation levels compared with the control group, and a downregulation of vimentin and upregulation of EGR1 protein expression. The present study demonstrated that miR-34a was deregulated in a highly invasive CRC cell lines, and that it may attenuate the migratory, invasive and proliferative capabilities of CRC cells by enhancing the expression of EGR1 and inhibiting that of vimentin. The results of the present study represent important progress towards understanding the mechanisms of CRC recurrence and metastasis.

Emerging Roles of lncRNAs in the Formation and Progression of Colorectal Cancer.

Colorectal cancer (CRC) is the primary cause of cancer-related death worldwide; however, specific and sensitive tools for the early diagnosis and targeted therapy of CRC are currently lacking. High-throughput sequencing technology revealed that gene expression of long-chain non-coding RNAs (lncRNAs) in a number of cancers directly or indirectly interferes with various biological processes. Emerging evidence suggests that lncRNAs regulate target genes and play an important role in the biological processes of malignancies, including CRC. Many carcinostatic/oncogenic lncRNAs have been identified as biomarkers for metastasis and prognosis in CRC; hence, they serve as therapeutic tools. In this article, we systematically review the literature on the disordered lncRNAs in CRC from four aspects: DNA transcription, RNA level regulation, post-translational level, and the translation of lncRNAs into polypeptides. Subsequently, we analyze the mechanism through which lncRNAs participate in the biological process of CRC. Finally, we discuss the application and prospects of these lncRNAs in CRC.

The mechanisms and clinical significance of PDCD4 in colorectal cancer.

In recent years, the incidence and mortality of colorectal cancer (CRC) have been on a global upward trend. There is an urgent need for effective tools to prevent and treat CRC and reduce morbidity and mortality of CRC patients. Recent evidence suggests that programmed cell death 4 (PDCD4), a novel tumor suppressor gene, inhibits tumor progression at transcriptional and translational levels and regulates multiple signal transduction pathways. However, little is known about the precise mechanisms regulating PDCD4 expression in CRC. In addition, several studies have demonstrated that the expression of in CRC is down-regulated or even absent. PDCD4 is therefore considered to be an independent prognostic factor in CRC and may be a potential support diagnostic tool for distinguishing in normal colon tissue, benign adenoma and CRC. This review will focus on the expression of PDCD4 in CRC and the relevant molecular mechanisms.

Characterization of CSF2A fusion gene and its effect on Epstein-Barr virus-positive tumor cells.

We build the latent membrane protein gene latent membrane protein 2A (LMP2A) and the granulocyte-macrophase colony-stimulating factor (GM-CSF) gene fusion gene (CSF2A) and discuss how the CSF2A fusion protein influenced the proliferation and apoptosis of Epstein-Barr virus-positive (EBV+ ) tumor cells. Reverse-transcription polymerase chain reaction (RT-PCR) method was used to amplify the LMP2A gene and GM-CSF gene fragments, respectively, according to the principle of overlap extension in the coding (Gly4Ser)3 polypeptide gene fragments of DNA restructured under the connection. The CSF2A gene could be connected with the pIRES2-enhanced green fluorescent protein vector by recombinant DNA technology and identified by enzyme electrophoresis analysis and DNA sequencing. Then, the recombinant vector was transfected into dendritic cells (DCs); RT-PCR and Western blot analysis were used for testing the CSF2A gene messenger RNA and protein expression. The impacts of CSF2A on the proliferation and apoptosis of EBV+ tumor cells were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and Hochest 33342 staining. We successfully obtained the recombinant vector named pIRES2-CSF2A. The expression of CSF2A could be detected by transfecting pIRES2-CSF2A into DCs. The DCs were cocultured with T lymphocytes and then acted on the EBV+ CNE2 nasopharyngeal carcinoma cells. MTT assay showed that the inhibiting effect of CSF2A obviously increased and the time dependency (**P < 0.01, *P < 0.05) also existed. Hochest 33342 staining showed apoptosis morphological changes of cells in nucleus staining and generated the apoptotic body. Apoptosis cells of the pIRES2-CSF2A group increased significantly at 48 hours. The results showed that the pIRES2-CSF2A recombinant vector was effectively transfected into DCs and the fusion gene CSF2A could promote EBV+ CNE2 cell apoptosis, laying the foundation for the specificity of EBV+ tumor targeting immune gene therapy in the future.

The function and clinical significance of eIF3 in cancer.

Abnormal regulation of gene expression is essential for tumorigenesis. Several studies indicate that regulation of oncogene expression and neoplastic transformation are controlled by subunits of eukaryotic translation initiation factors (eIFs). Eukaryotic translation initiation factor 3 (eIF3) is the largest (800 kDa) and the most complex mammalian initiation factor. It is composed of 13 non-identical polypeptides designated as eIF3a-m and plays a pivotal role in protein synthesis that bridges the 43S pre-initiation complex and eIF4F-bound mRNA. However, the functional roles of individual subunits are not yet very clear. This review presents on several of aberrant expressed eIF3 subunits which are detected in various human cancers and the associated mechanisms have been acknowledged or are still not sure. Finally, identifying novel targets and biomarkers for caner is of great importance in early diagnosis and treatment of cancer. eIF3 may be a novel target molecule in drug development for cancer treatment and prevention.