Targeting methyltransferase-like 5-mediated sphingomyelin metabolism: A novel therapeutic approach in gastric cancer.

Gastric cancer (GC) is a global health problem and a leading cause of cancer-related deaths, with its mortality rate ranking third among all cancers. The etiology and progression of GC are characterized by a complex interplay of genetic and epigenetic changes, which present challenges for its early diagnosis and effective treatment. Elucidating the mechanisms underlying the occurrence and development of GC and identifying novel biomarkers for early detection and prognosis are crucial to improving patient outcomes.

Optimizing postsurgical recovery for elderly patients with gastric cancer.

Based on a recent study by Li , this editorial examines the significance of enhanced recovery after surgery (ERAS) protocols for elderly patients with gastric cancer. Cancer-related mortality, which is overwhelmingly caused by gastric cancer, calls for effective treatment strategies. Despite advances in the field of oncology, conventional postoperative care often results in prolonged hospital stays and increased complications.

Retroperitoneal bronchogenic cyst: A case report and review of literature.

Background: Bronchogenic cysts are rare developmental anomalies that belong to the category of congenital enterogenous cysts. They arise from lung buds and are present at birth. The embryonic foregut is their origin.

H19 encourages aerobic glycolysis and cell growth in gastric cancer cells through the axis of microRNA-19a-3p and phosphoglycerate kinase 1.

Numerous studies have been conducted on long non-coding RNAs (lncRNAs) in human tumors like gastric cancer (GC). Our research uncovers how aerobic glycolysis and cell proliferation in gastric cancer cells are related to H19. We discovered that H19 was highly expressed in tumor tissues and that patients with higher H19 expression have a poorer prognosis.

Long non-coding RNAs and pancreatic cancer: A multifaceted view.

Pancreatic cancer (PC) is a highly malignant disease with a 5-year survival rate of only 10%. Families with PC are at greater risk, as are type 2 diabetes, pancreatitis, and other factors. Insufficient early detection methods make this cancer have a poor prognosis.

Bioinformatic and experimental analyses of key biomarkers in pancreatic cancer.

The present study aimed to screen the key genes in pancreatic cancer and to explore the pathogenesis of pancreatic cancer. A total of three expression profiling datasets (GSE28735, GSE16515 and GSE15471) associated with pancreatic cancer were retrieved from the public gene chip database. The differentially expressed genes (DEGs) were screened by GEO2R and subjected to Gene Ontology (GO) and signaling pathway enrichment analysis.

Identification of G-protein signaling modulator 2 as a diagnostic and prognostic biomarker of pancreatic adenocarcinoma: an exploration of its regulatory mechanisms.

Background: Pancreatic adenocarcinoma (PAAD) has a high rate of mortality. Unfortunately, it is difficult to diagnosis. This study aimed to develop a more in-depth understanding of the disease.

LncRNA SNHG15 Contributes to Immuno-Escape of Gastric Cancer Through Targeting miR141/PD-L1.

Introduction: Long non-coding RNAs (lncRNAs) have been demonstrated to participate in many biological processes and severs as important regulators during the progression of gastric cancer.

Methods: Here, we introduced human lncRNA SNHG15 which was highly expressed in gastric cancer and cells. Interestingly, the expression of SNHG15 was correlated with programmed cell death ligand 1 (PD-L1), which promotes the resistance of gastric cancer cells to immune responses.

Expression profile of lncRNAs and mRNAs in intestinal macrophages.

Non-coding RNAs (ncRNAs) have been previously reported to serve an important role in transcription. In addition, several studies have revealed that long ncRNAs (lncRNAs) have a crucial role in human diseases. However, the association between lncRNAs and inflammation‑induced intestinal macrophages in the intestinal mucosal barrier has remained elusive.

Netrin-1 promotes cell neural invasion in gastric cancer via its receptor neogenin.

Neural invasion (NI) is one of the important routes for local spread of gastric cancer (GC) correlated with poor prognosis. However, the exact cellular characteristics and molecular mechanisms of NI in GC are still unclear. Netrin-1(NTN1) as an axon guidance molecule was firstly found during neural system development.

MicroRNA-505 suppresses gastric cancer cell proliferation and invasion by directly targeting Polo-like kinase-1.

Purpose: The expression of microRNA-505 (miR-505) has been investigated in various cancers; however, its effect and mechanism in relation to gastric cancer (GC) are yet to be determined. Thus, the current evaluation aimed to examine the expression and potential role of miR-505 in GC.

Materials And Methods: Quantitative real-time PCR was carried out to analyze miR-505 expression in GC cells and tissues.

G-protein-signaling modulator 2 expression and role in a CD133 pancreatic cancer stem cell subset.

Background: To investigate the expression and role of G-protein-signaling modulator 2 (GPSM2) in a CD133 pancreatic stem cell subset.

Materials And Methods: Pancreatic cancer stem cells (PCSCs) from the cell line PANC-1 were sorted into CD133 and CD133 subsets by flow cytometry. The tumorigenic potential of the subsets was assessed by subcutaneous tumor formation experiments in nude mice.

[Corrigendum] Netrin‑1 induces the proliferation of gastric cancer cells via the ERK/MAPK signaling pathway and FAK activation.

During the preparation of the figures in the above article, the authors inadvertently selected images for the shCTL experiments portrayed in Fig. 5I and J (for the MGC803 and SGC7901 cell lines, respectively) that were generated from the same original data source. A corrected version of Fig.

PLK1 as a potential prognostic marker of gastric cancer through MEK-ERK pathway on PDTX models.

Background: PLK1 has been identified as having a great effect on cell division and maintaining genomic stability in mitosis, spindle assembly, and DNA damage response by current studies.

Materials And Methods: We assessed PLK1 expression in cervical cancer tissues and cells. We have also evaluated the effects of PLK1 on gastric cancer cell proliferation, migration, and apoptosis both in vitro and in vivo.

Netrin‑1 induces the proliferation of gastric cancer cells via the ERK/MAPK signaling pathway and FAK activation.

Netrin‑1 (NTN1) has been demonstrated to promote tumorigenesis in multiple types of cancer; however, its role in the growth of gastric cancer (GC) cells has not been described in detail. In the present study, the data suggested that NTN1 knockdown significantly decreased the proliferation of GC cells, whereas NTN1 overexpression had an opposing effect. Furthermore, the use of focal adhesion kinase (FAK) inhibitor decreased the proliferation of GC cells.

Netrin-1 promotes metastasis of gastric cancer by regulating YAP activity.

Yes-associated protein (YAP) is a major downstream molecular of the Hippo pathway, which plays important role in cancer development. Netrin-1 conveys oncogenic activity in many types of malignant tumors. However, the downstream signaling of netrin-1 mediating its oncogenic effects in gastric cancer (GC) is not well defined.

Giant mucinous adenocarcinoma of the appendix: a case report.

Background: Appendiceal mucinous adenocarcinoma is an extremely rare disease in clinical practice. Here, we report a case of unprecedented size that occupied the entire abdomen of a man.

Case Presentation: A 49-year-old Chinese Han man presented with symptoms of abdominal distension.

YEATS4 promotes the tumorigenesis of pancreatic cancer by activating beta-catenin/TCF signaling.

Beta-catenin/TCF signaling has been reported to promote the growth and metastasis of pancreatic cancer cells. However, the regulation for the beta-catenin/TCF transcriptional complex remains largely unknown. Here, we have found that YEATS4 is a positive regulator for Beta-catenin/TCF signaling.

[Interferon regulatory factor 5(IRF5) regulates the differentiation of bone marrow-derived macrophages in mice].

Objective: To investigate the expression differences of interferon regulatory factor 5( IRF5) between M1 and M2 macrophages derived from mouse bone marrow and the effects of small interfering RNA targeting IRF5 gene( IRF5siRNA) on macrophage differentiation.

Methods: With the treatment of IFN-γ and lipopolysaccharide( LPS),mouse bone marrow-derived macrophages were differentiated into M1 macrophages; while with the treatment of IL-4,mouse bone marrow-derived macrophages were differentiated into M2 macrophages. Differentiation efficiency was measured by flow cytometry.

IRF5 regulates lung macrophages M2 polarization during severe acute pancreatitis .

Aim: To investigate the role of interferon regulatory factor 5 (IRF5) in reversing polarization of lung macrophages during severe acute pancreatitis (SAP) .

Methods: A mouse SAP model was established by intraperitoneal (ip) injections of 20 μg/kg body weight caerulein. Pathological changes in the lung were observed by hematoxylin and eosin staining.

CARF activates beta-catenin/TCF signaling in the hepatocellular carcinoma.

Overactivation of Ras signaling is very common in the hepatocellular carcinoma (HCC) due to its constitutive active mutation, which makes it a big challenge to target Ras signaling. Therefore, identifying effectors downstream of Ras signaling would benefit the development of novel therapeutic strategies. In this study, it was found that the expression of CARF (collaborate of ARF) was induced by oncogenic RasV12.

FOXC2 is up-regulated in pancreatic ductal adenocarcinoma and promotes the growth and migration of cancer cells.

The transcriptional factor Forkhead box protein C2 (FOXC2) was recently demonstrated to be up-regulated in various cancer types. However, its expression profile and the biological functions in pancreatic cancer remain unknown. In this study, we examined the expression pattern of FOXC2 in pancreatic ductal adenocarcinoma (PDAC) tissues and investigated the functions of FOXC2 in the progression of PDAC.

Secreted protein acidic and rich in cysteine enhances the chemosensitivity of pancreatic cancer cells to gemcitabine.

It has been previously shown that the simultaneous exposure of colon cancer cells MIP to irinotecan and secreted protein acidic and rich in cysteine (SPARC) enhances anticancer activity. However, whether there is same effect of SPARC in pancreatic cancer remains largely unknown. Therefore in this study, we aimed to investigate the role of SPARC played in the sensitivity of pancreatic cancer to gemcitabine.