ATF4-mediated circTDRD3 promotes gastric cancer cell proliferation and metastasis by regulating the miR-891b/ITGA2 axis and AKT signaling pathway.

BACKGROUND: Gastric cancer (GC) is a cancer of the gastrointestinal tract that is highly malignant and has poor prognosis. Circular RNAs are a class of nonclassical RNA molecules that have been determined to be involved in GC malignancy in various ways. However, the underlying function and mechanism of circTDRD3 in gastric cancer remain largely unknown. METHODS: We analyzed circTDRD3 expression in databases and verified the findings in GC cell lines and tissue specimens. A series of functional gene overexpression and knockdown assays in vivo and in vitro were carried out to investigate the role of circTDRD3 in proliferation and metastasis. Here, we revealed the role of the miR-891b/ITGA2 axis by analyzing bioinformatics datasets. Furthermore, we performed dual-luciferase, fluorescence in situ hybridization, RNA pull-down, and functional rescue experiments to examine the relationships between circTDRD3 and its interacting molecules. Western blot confirmed the positive regulatory role of circTDRD3 in the AKT signaling pathway. A promoting effect of ATF4 on circTDRD3 was determined through chromatin immunoprecipitation. RESULTS: CircTDRD3 was significantly overexpressed in GC tissues compared with adjacent benign tissue, and its expression level was positively correlated with tumor volume and lymph node metastasis. CircTDRD3 promoted GC cell proliferation and migration in vitro and in vivo. Mechanistically, circTDRD3 exerted a tumor-promoting effect by regulating the miR-891b/ITGA2 axis and AKT signaling pathway in a positive feedback manner mediated by the transcription factor ATF4. CONCLUSIONS: ATF4-mediated circTDRD3 overexpression modulates the proliferation and metastasis of GC cells through the miR-891b/ITGA2 axis in a positive feedback manner.

A phase II study of perioperative treatment in gastric cancer with No.16a2/b1 lymph node metastasis: DRAGON-06 trial.

Although gastric cancer with para-aortic lymph node (PAN) metastasis is commonly regarded as unresectable, surgeons have explored the optimal treatment for patients with PAN metastases limited to No.16a2/b1 in the past few decades. Preoperative systemic therapy combined with D2 gastrectomy plus PAN dissection may improve the prognosis of these patients. In this multicenter phase II trial, 29 gastric cancer patients with PAN metastasis limited to No.16a2/b1 will receive preoperative treatment with nab-paclitaxel, oxaliplatin, S-1 (nab-POS: nab-paclitaxel, oxaliplatin, S-1) and sintilimab followed by D2 gastrectomy plus PAN dissection; and postoperative treatment with oral S-1, intravenous sintilimab and intraperitoneal paclitaxel. The end points for the study are 3-year overall survival, 3-year disease-free survival, pathological response rate, incidence of postoperative complications and adverse events.

Stomach cancer with metastases in the para-aortic lymph nodes is usually considered inoperable. Chemotherapy combined with resection of the stomach and more extensive lymph node dissection may prolong the life of these patients. In this multicenter study, 29 stomach cancer patients with para-aortic lymph node metastases will receive preoperative treatment with nab-paclitaxel, oxaliplatin, S-1 and sintilimab, followed by resection of the stomach combined with para-aortic lymph node dissection and use of continued oral, intravenous and intraperitoneal chemotherapy. The study's end points are 3-year overall survival, 3-year disease-free survival, pathological response rate, incidence of postoperative complications and adverse events. Clinical Trial Registration: ChiCTR2200061125 (ChiCTR.org.cn).

Inhibition of miR-16 Ameliorates Inflammatory Bowel Disease by Modulating Bcl-2 in Mouse Models.

BACKGROUND: In recent years, microRNA (miRNA) is considered as a potential therapy target. To study the regulatory mechanism and therapeutic effect of miRNAs on inflammatory bowel disease (IBD), we investigated microRNAs that regulate apoptosis-related protein B cell lymphoma-2 (Bcl-2). We examined the role of miR-16 in IBD and the effect of inhibiting the expression of miR-16 on disease progression. MATERIALS AND METHODS: Dextran sulfate sodium was used to induce ulcerative colitis in mice. RNA and protein were extracted from the rectal mucosa of mice. Real-time quantitative polymerase chain reaction and Western blotting were used to detect the expression of miR-16 and Bcl-2. The effects of miR-16 on intestinal mucosal immunity were studied by real-time quantitative polymerase chain reaction, and inflammatory factors such as interleukin-1ß, interleukin-6, and tumor necrosis factor-α were detected. The weight changes, disease activity index, length of the rectal colon, and pathological score of the mice were used to evaluate the effect of inhibiting miR-16 on disease progression. Through the establishment of overexpression and low expression cell lines of miR-16, the regulation of miR-16 on Bcl-2 was studied. RESULTS: MiR-16 was overexpressed in the IBD model, whereas Bcl-2 had lower expression in the mucosa. Inhibiting expression of miR-16 significantly decreased the expression of interleukin-1ß, interleukin-6, and tumor necrosis factor-α. In mice, the weight change, disease activity index, and pathological score decreased in the experimental group, in which miR-16 was inhibited. High expression of miR-16 can inhibit Bcl-2 expression. CONCLUSIONS: MiR-16 plays a critical role in IBD via Bcl-2 and is a promising target in IBD therapy.

Lin28: an emerging important oncogene connecting several aspects of cancer.

RNA-binding protein Lin28 was originally found as a heterochronic gene which played a significant role in the development of Caenorhabditis elegans. The tumor suppressor let-7 is a downstream target of Lin28, which has a wide variety of target genes which are involved in many aspects of cellular activities. By inhibition of let-7 and directly binding the target RNAs, Lin28 plays an important role in different biological and pathological processes including differentiation, metabolism, proliferation, pluripotency, and tumorigenesis. Overexpression of Lin28 has been reported in several kinds of cancers and is correlated with poor outcomes. It has been shown that Lin28 could affect the progression of cancers in several ways, such as promoting proliferation, increasing glucose metabolism, and inducing epithelial-mesenchymal transition (EMT) and cancer stem cells. Decrease of Lin28 expression or reactivation of let-7 in cancer cells could induce a reverse effect, indicating their therapeutic values in developing novel strategies for cancer treatment. Here, we will overview the regulatory mechanisms and functions of Lin28 in cancers.

Dysregulation of TTP and HuR plays an important role in cancers.

Defects in the adenosine-uridine (AU)-rich elements (AREs), which mediate post-transcriptional regulation, play important roles in cancers. Both tristetraprolin (TTP, also known as TIS11 and ZFP36) and human antigen R (HuR, also known as ELAVL1) are two important and closely related AU-rich RNA-binding proteins (ARE-BPs). High-expression or aberrant nuclear/cytoplasmic distribution of HuR and decreased TTP have been found in many types of cancers. TTP mediates the decay of target mRNAs, whereas HuR generally stabilizes target transcripts and promotes translation of certain mRNAs. Furthermore, thousands of overlapping binding sites of TTP and HuR were found in more than 1300 genes. RNA-IP experiments also indicated that TTP can bind directly to and destabilize HuR mRNA. The dysregulation of TTP and HuR has been found to play an important role in the progression of cancers, including inflammation-related cancer, as well as in proliferation, apoptosis, angiogenesis, metastasis, invasion, and chemotherapy resistance. In this review, we provided an overview of the role of TTP and HuR, as well as the underlying mechanisms of the TTP-HuR axis in cancers.

The cross talk between long, non-coding RNAs and microRNAs in gastric cancer.

Gastric cancer is one of the most common malignant diseases and remains the second leading cause of cancer-related mortality worldwide. Although great effort has been made during the past decades to facilitate the early detection and treatment of gastric cancer, the prognosis is not yet satisfactory and the underlying molecular mechanisms of gastric cancer pathogenesis are not fully understood. Meanwhile, non-coding RNAs have been established as key players in regulating various biological and pathological processes, such as cell-cycle progression, chromatin remodeling, gene transcription, and posttranscriptional processing. Furthermore, numerous studies have also revealed a complicated interplay among different species of non-coding RNAs; therefore, the cross-regulation between long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) has begun to emerge. This lncRNA-miRNA cross talk, which has attracted increasing attention in recent years, is involved in a great number of human diseases including gastric cancer. In this review, we summarize the latest research progress of the interactions between lncRNAs and miRNAs, highlighting their influences on the development and progression of gastric cancer to provide novel approaches for cancer diagnosis and treatment.

Long non-coding RNAs: emerging players in gastric cancer.

Gastric cancer (GC) remains a major public health issue as the second leading cause of cancer-related death and the fourth most common cancer worldwide. Although much progress has been achieved in recent years, the early diagnosis and treatment for GC are not yet satisfactory; thus, the prognosis remains poor. Therefore, identification of novel molecules for early diagnosis, prognosis, and treatment is urgently needed. Long non-coding RNAs (lncRNAs) are a new class of non-coding RNAs that participate in a variety of biological processes such as cell proliferation, cell cycle, differentiation, and apoptosis, mainly by regulation of gene expression at various levels, including chromatin, splicing, transcriptional, and post-transcriptional levels. Some lncRNAs are upregulated in cancer and possess oncogenic properties, while others exhibit aberrant low expression and act as tumor suppressors. In this review, we overview the functional roles and regulatory mechanisms of lncRNAs in GC and evaluate their diagnostic, prognostic, and therapeutic values.

The lncRNA-MYC regulatory network in cancer.

Long non-coding RNAs (lncRNAs) have been widely studied in recent years, and accumulating evidence identified lncRNAs as crucial regulators of various biological processes, including cell cycle progression, chromatin remodeling, gene transcription, and posttranscriptional processing. In addition, the fact that lncRNAs interact with the MYC gene family in human carcinomas has been discovered. This review summarizes the latest progress on the investigation of lncRNAs and MYC, particularly focusing on the interplay between lncRNAs and MYC in cancer to reveal the significance of lncRNA-MYC network in regulating initiation, development, and metastasis of tumors. Further research and collection of clinical data would provide a better understanding of lncRNA-MYC network in cancer diagnosis and treatment.

Exhaled breath and urinary volatile organic compounds (VOCs) for cancer diagnoses, and microbial-related VOC metabolic pathway analysis: a systematic review and meta-analysis.

BACKGROUND: The gradual evolution of the detection and quantification of volatile organic compounds (VOCs) has been instrumental in cancer diagnosis. The primary objective of this study was to assess the diagnostic potential of exhaled breath and urinary VOCs in cancer detection. As VOCs are indicative of tumor and human metabolism, our work also sought to investigate the metabolic pathways linked to the development of cancerous tumors. MATERIALS AND METHODS: An electronic search was performed in the PubMed database. Original studies on VOCs within exhaled breath and urine for cancer detection with a control group were included. A meta-analysis was conducted using a bivariate model to assess the sensitivity and specificity of the VOCs for cancer detection. Fagan's nomogram was designed to leverage the findings from our diagnostic analysis for the purpose of estimating the likelihood of cancer in patients. Ultimately, MetOrigin was employed to conduct an analysis of the metabolic pathways associated with VOCs in relation to both human and/or microbiota. RESULTS: The pooled sensitivity, specificity and the area under the curve for cancer screening utilizing exhaled breath and urinary VOCs were determined to be 0.89, 0.88, and 0.95, respectively. A pretest probability of 51% can be considered as the threshold for diagnosing cancers with VOCs. As the estimated pretest probability of cancer exceeds 51%, it becomes more appropriate to emphasize the 'ruling in' approach. Conversely, when the estimated pretest probability of cancer falls below 51%, it is more suitable to emphasize the 'ruling out' approach. A total of 14, 14, 6, and 7 microbiota-related VOCs were identified in relation to lung, colorectal, breast, and liver cancers, respectively. The enrichment analysis of volatile metabolites revealed a significant enrichment of butanoate metabolism in the aforementioned tumor types. CONCLUSIONS: The analysis of exhaled breath and urinary VOCs showed promise for cancer screening. In addition, the enrichment analysis of volatile metabolites revealed a significant enrichment of butanoate metabolism in four tumor types, namely lung, colorectum, breast and liver. These findings hold significant implications for the prospective clinical application of multiomics correlation in disease management and the exploration of potential therapeutic targets.

The role of LncRNA-mediated autophagy in cancer progression.

Long non-coding RNAs (lncRNAs) are a sort of transcripts that are more than 200 nucleotides in length. In recent years, many studies have revealed the modulatory role of lncRNAs in cancer. Typically, lncRNAs are linked to a variety of essential events, such as apoptosis, cellular proliferation, and the invasion of malignant cells. Simultaneously, autophagy, an essential intracellular degradation mechanism in eukaryotic cells, is activated to respond to multiple stressful circumstances, for example, nutrient scarcity, accumulation of abnormal proteins, and organelle damage. Autophagy plays both suppressive and promoting roles in cancer. Increasingly, studies have unveiled how dysregulated lncRNAs expression can disrupt autophagic balance, thereby contributing to cancer progression. Consequently, exploring the interplay between lncRNAs and autophagy holds promising implications for clinical research. In this manuscript, we methodically compiled the advances in the molecular mechanisms of lncRNAs and autophagy and briefly summarized the implications of the lncRNA-mediated autophagy axis.

Identification of TAP1 as a T-cell related therapeutic target in gastric cancer by mediating oxalipliatin-related synergistic enhancement of immunotherapy.

BACKGROUND: Given the intricate molecular complexities and heterogeneity inherent in T-cell immunotherapy of gastric cancer (GC), elucidative T-cell-related biomarkers were imperative needed for facilitating the prediction of GC patient prognosis and identify potential synergistic therapeutic targets. METHODS: We conducted COX regression analysis in TISIDB, TCGA-STAD, and GEO databases to identify 19 GC T-cell-mediated sensitivity tumor killing (TTK) genes (key GCTTKs). Based on key GCTTKs, we constructed two TTK patterns and analyzed their metabolic pathways, mutation features, clinical data distribution, immune cell infiltration, and prognosis. LASSO regression was performed to develop a T-cell-mediated GC Prognosis (TGCP) model. We validated the TGCP model in GC patients. TAP1 was further selected for investigation of its biological functions and molecular mechanisms. We assessed the potential of TAP1 as a promising therapeutic target for GC using Patient-derived organoids (PDOs)-derived xenografts (PDOXs) models of GC. RESULTS: The TTK patterns display notable disparities. The TGCP model showcases its proficiency in predicting immune response efficacy, effectively distinguishes immunotherapy difference GC patients. Our findings find further confirmation in PDOX models, affirming TAP1 can enhance immunotherapy facilitated by PDL1 inhibitors. Furthermore, Oxaliplatin, by promoting TAP1 expression, augments PDL1 expression, thereby enhancing the efficacy of immunotherapy. CONCLUSIONS: We constructed a TGCP model, which demonstrates satisfactory predictive accuracy. Out of 9 prognostic genes, TAP1 was validated as a synergistic target for Oxaliplatin and PDL1 inhibitors, offering a genetic-level explanation for the synergy observed in GC treatment involving Oxaliplatin in combination with PDL1 inhibitors.

H3K18 lactylation-mediated VCAM1 expression promotes gastric cancer progression and metastasis via AKT-mTOR-CXCL1 axis.

The role of the Immunoglobulin Superfamily (IgSF) as adhesion molecules in orchestrating inflammation is pivotal, yet its specific involvement in gastric cancer (GC) remains unknown. We analyzed IgSF components and discerned conspicuously elevated VCAM1 expression in GC, correlating with a poor prognosis. Remarkably, VCAM1 enhances GC cell proliferation and migration by activating AKT-mTOR signaling. Moreover, lactate in the tumor microenvironment (TME) promotes dynamic lactylation of H3K18 (H3K18la), leading to transcriptional activation of VCAM1 in GC cells. Furthermore, VCAM1 actively mediates intercellular communication in the TME. AKT-mTOR-mediated CXCL1 expression is increased by VCAM1, facilitating the recruitment of human GC-derived mesenchymal stem cells (hGC-MSCs), thereby fostering immunesuppression and accelerating cancer progression. In summary, H3K18 lactylation upregulated VCAM1 transcription, which activated AKT-mTOR signaling, and promoted tumor cell proliferation, EMT Transition and tumor metastasis. VCAM1 upregulated CXCL1 expression by AKT-mTOR pathway, so as to facilitate hGC-MSCs and M2 macrophage recruitment and infiltration. These findings provide novel therapeutic targets for GC.

Biomimicking covalent organic frameworks nanocomposite coating for integrated enhanced anticorrosion and antifouling properties of a biodegradable magnesium stent.

The utilization of biodegradable magnesium (Mg) alloys in the fabrication of temporary non-vascular stents is an innovative trend in biomedical engineering. However, the heterogeneous degradation profiles of these biomaterials, together with potential bacterial colonization that could precipitate infectious or stenotic complications, are critical obstacles precluding their widespread clinical application. In pursuit of overcoming these limitations, this study applies the principles of biomimicry, particularly the hydrophobic and anti-fouling characteristics of lotus leaves, to pioneer the creation of nanocomposite coatings. These coatings integrate poly-trimethylene carbonate (PTMC) with covalent organic frameworks (COFs), to modify the stent's surface property. The strategic design of the coating's topography, porosity, and self-polishing capabilities collectively aims to decelerate degradation processes and minimize biological adhesion. The protective qualities of the coatings were substantiated through rigorous testing in both in vitro dynamic bile tests and in vivo New Zealand rabbit choledochal models. Empirical findings from these trials confirmed that the implementation of COF-based nanocomposite coatings robustly fortifies Mg implantations, conferring heightened resistance to both biocorrosion and biofouling as well as improved biocompatibility within bodily environments. The outcomes of this research elucidate a comprehensive framework for the multifaceted strategies against stent corrosion and fouling, thereby charting a visionary pathway toward the systematic conception of a new class of reliable COF-derived surface modifications poised to amplify the efficacy of Mg-based stents. STATEMENT OF SIGNIFICANCE: Biodegradable magnesium (Mg) alloys are widely utilized in temporary stents, though their rapid degradation and susceptibility to bacterial infection pose significant challenges. Our research has developed a nanocomposite coating inspired by the lotus, integrating poly-trimethylene carbonate with covalent organic frameworks (COF). The coating achieved self-polishing property and optimal surface energy on the Mg substrate, which decelerates stent degradation and reduces biofilm formation. Comprehensive evaluations utilizing dynamic bile simulations and implantation in New Zealand rabbit choledochal models reveal that the coating improves the durability and longevity of the stent. The implications of these findings suggest the potential COF-based Mg alloy stent surface treatments and a leap forward in advancing stent performance and endurance in clinical applications.

FAM117B promotes gastric cancer growth and drug resistance by targeting the KEAP1/NRF2 signaling pathway.

Gastric cancer often shows malignant growth and insensitivity to chemotherapeutic drugs due to the regulation of complex molecular mechanisms, which results in poor prognosis for patients. However, the relevant molecular mechanisms remain unclear. In this study, we reported that family with sequence similarity 117, member B (FAM117B), promoted the growth of gastric cancer cells and reduced the sensitivity of cells to chemotherapeutic drugs. Mechanistically, FAM117B competed with nuclear factor E2-related factor 2 (NRF2) for Kelch-like ECH-associated protein 1 (KEAP1) binding, reduced the ubiquitination degradation of NRF2, and activated the KEAP1/NRF2 signaling pathway. Moreover, FAM117B-induced growth and chemoresistance of gastric cancer cells were NRF2 dependent. We found that FAM117B and NRF2 protein levels were highly expressed in tumor tissues of patients with gastric cancer and their co-overexpression represented an independent factor for poor prognosis. Collectively, our findings reveal that FAM117B is involved in promoting gastric cancer growth and drug resistance, and it could be exploited as a cancer therapeutic target.

The characteristics, tumorigenicities and therapeutics of cancer stem cells based on circRNAs.

Currently, recurrence and metastasis are still the main causes leading to the failure of various therapies for malignant tumors. In view of this, research on cancer stem cells (CSCs) has received increasing attention. CSCs are a subgroup of cancer cells with the characteristics of self-renewal, multidirectional differentiation, and immortal proliferation, and are closely related to resistance, metastasis, and recurrence. Circular RNAs (circRNAs) are a type of noncoding RNA (ncRNA) containing a covalent closed loop and are characterized by their abundance, stability, conservation, and tissue specificity. In this article, we focus on the characteristics of CSCs and review the latest research advances on the role of circRNAs in CSCs.

Nebulization Therapy with Umbilical Cord Mesenchymal Stem Cell-Derived Exosomes for COVID-19 Pneumonia.

BACKGROUND: Scientists have been facing numerous challenges in the development of an effective therapeutic strategy for the treatment of COVID-19 pneumonia. Several studies have suggested that improving patient immunity and reducing lung injury induced by SARS-CoV-2 may be effective for treating patients with COVID-19. METHODS: A pilot trial of nebulization therapy with exosomes of mesenchymal stem cells (MSCs) was performed on seven patients with COVID-19 pneumonia. Exosomes secreted from MSCs were collected and purified using multiple ultrafiltration steps. All patients were treated with nebulization of MSC-derived exosomes, and primary safety and efficacy outcomes were evaluated. RESULTS: Our clinical study demonstrated that nebulization of MSC-derived exosomes is a novel method that might be utilized in the treatment of COVID-19 pneumonia. Nebulization of MSC-derived exosomes did not induce acute allergic or secondary allergic reactions but did promote the absorption of pulmonary lesions and reduce the duration of hospitalization for mild cases of COVID-19 pneumonia. CONCLUSIONS: Nebulization of MSC-derived exosomes is a safe, effective, and simple method, and their application at the beginning of treatment may be more beneficial. TRIAL REGISTRATION: Chinese Clinical Trial Registry, ChiCTR2000030261. Registered on 26 February 2020.

A pan-cancer analysis of the expression of STAT family genes in tumors and their relationship to the tumor microenvironment.

Background: The signal transducer and activator of transcription (STAT) protein family, a group of seven members (STAT1, STAT2, STAT3, STAT4, STAT5A, STAT5B, and STAT6), has been widely used to investigate numerous biological functions including cell proliferation, differentiation, apoptosis, and immune regulation. However, not much is known about the role of the STAT family genes in pan-cancer. Methods: Tumor Immune Estimation Resource (TIMER), Sangerbox, cBioPortal, GSCALite, Xena Shiny, GeneMANIA, Gene Expression Profiling Interactive Analysis (GEPIA), and Metascape were used to analyze the relationship between STAT gene expression, clinical outcome, gene variation, methylation status, pathway activity, tumor immune infiltration, and microenvironment in different cancer types and screened drugs that could potentially influence STATs. Results: The Cancer Genome Atlas (TCGA) pan-cancer data showed that most STAT family genes were extensively changed in most tumors compared to the adjacent normal tissues. We also found that STAT gene expression could be used to predict patient survival in various cancers. The STAT gene family formed a network of interaction networks that was associated with several pathways. By mining the of Genomics Drug Sensitivity in Cancer (GDSC) database, we discovered a number of potential drugs that might target STAT regulators. Importantly, the close correlation between STATs and immunocell infiltration suggested the important role of dysregulation of STATs in tumor immune escape. Finally, the relation between STAT gene expression and the tumor microenvironment (TME) indicated that the higher expression of STAT regulators, the higher the degree of tumor stem cells. Conclusion: Considering these genomic alterations and clinical features of STAT family members across cancer types, it will be possible to change the relationship between STATs and tumorigenesis. It was beneficial to treat cancer by targeting these STAT regulators.

Controlled release of hydrogen by implantation of magnesium induces P53-mediated tumor cells apoptosis.

Hydrogen has been used to suppress tumor growth with considerable efficacy. Inhalation of hydrogen gas and oral ingestion of hydrogen-rich saline are two common systemic routes of hydrogen administration. We have developed a topical delivery method of hydrogen at targeted sites through the degradation of magnesium-based biomaterials. However, the underlying mechanism of hydrogen's role in cancer treatment remains ambiguous. Here, we investigate the mechanism of tumor cell apoptosis triggered by the hydrogen released from magnesium-based biomaterials. We find that the localized release of hydrogen increases the expression level of P53 tumor suppressor proteins, as demonstrated by the in vitro RNA sequencing and protein expression analysis. Then, the P53 proteins disrupt the membrane potential of mitochondria, activate autophagy, suppress the reactive oxygen species in cancer cells, and finally result in tumor suppression. The anti-tumor efficacy of magnesium-based biomaterials is further validated in vivo by inserting magnesium wire into the subcutaneous tumor in a mouse. We also discovered that the minimal hydrogen concentration from magnesium wires to trigger substantial tumor apoptosis is 91.2 µL/mm3 per day, which is much lower than that required for hydrogen inhalation. Taken together, these findings reveal the release of H2 from magnesium-based biomaterial exerts its anti-tumoral activity by activating the P53-mediated lysosome-mitochondria apoptosis signaling pathway, which strengthens the therapeutic potential of this biomaterial as localized anti-tumor treatment.

MicroRNA-149: A review of its role in digestive system cancers.

MicroRNAs (miRNAs) are a group of highly conserved, short (18-25 nucleotide long) non-coding RNAs which play important functional roles in cellular differentiation, biological development, pathogenesis and disease susceptibility and have been linked to both tumorigenesis and the malignant progression of various cancers. miRNAs primarily exert their function through the negative regulation of their target gene's transcription via the specific recognition of their 3' untranslated region. A single miRNA can regulate multiple target genes and most miRNAs are controlled by several factors. Recent studies have shown that microRNA-149 (miR-149) plays a pivotal role in the pathogenesis of digestive system cancers and may act as a potential diagnostic marker and therapeutic target. In this review, we summarize and discuss the most recent reports describing miR-149 in digestive system cancers, including its single nucleotide polymorphisms, expression levels, target genes, drug sensitivity and clinical significance.

3D Printing Technology Improves Medical Interns' Understanding of Anatomy of Gastrocolic Trunk.

OBJECTIVE: Complex vascular anatomy has always been a difficult point for medical students. Gastrocolic trunk (Henle trunk) has many branches and variations, involving the venous reflux of the stomach, right colon, and pancreas. This study investigated the effects of 3 dimensional (3D) printing technology on medical interns' understanding of Henle trunk's variation, by comparing 2 dimensional (2D) images. SETTING: Henle trunk modes were manufactured using 3D-CT angiography and 3D-printing technology. PARTICIPANTS: Forty-seven interns from 2 medical schools (Nanjing Medical University and Medical College of Nantong University) participated in the study. DESIGN: The interns were divided randomly allocated into 2 groups, where group 1 was the control group with a 2D image of Henle trunk plus surgical video (named 2D image group), and group 2 was the study group with a 3D printed model of Henle trunk plus surgical video (named 3D-printing group). Knowledge of interns on the Henle trunk was compared between 2 groups using a question test before and after the teaching intervention. RESULTS: All interns had an improved overall assessment score as a result of attending the seminar, whether in the 2D image group or the 3D-printing group. The score of the 2D image group increased 32.57 ± 13.86, and the 3D-printing group increased 47.04 ± 12.99, showing significant difference (p = 0.001). There was no significant difference observed between postseminar scores between 2 medical schools (p = 0.975). There was a significant improvement in satisfaction among the 3D-printing group for education depth, novel and inspiring of teaching method, except for the interaction between teacher and interns (p = 0.215). Interns hope to have more teaching time for 3D printing, and not satisfied with the time of 3D printing teaching compared with those in the 2D image group (p = 0.021). CONCLUSIONS: The 3-D printed Henle trunk model is a very effective teaching tool, which can help interns understand the anatomy of Henle trunk. The application of 3D printing technology in the teaching of interns of complex vascular anatomy is worth popularizing in teaching hospitals.