The purpose of this study was to assess the anti-tumor effects of macrophage migration inhibitory factor (MIF) siRNA on colorectal cancer in a mouse xenograft model. MIF specific siRNA (MIF siRNA) or a nonspecific control siRNA was introduced to murine colorectal cancer CT-26 cells. Mouse xenograft models of colorectal cancer were established. MIF siRNA, control siRNA or water was injected twice a week intravenously for 4 weeks. MIF siRNA inhibited the proliferation and migration, while induced apoptosis of CT-26 cells . Injection of MIF siRNA resulted in a significant decrease of serum MIF and VEGF levels, and the weight and volume of cecum-grafted tumors . In contrast, the number of apoptotic cells and caspase-3 expression were increased by MIF siRNA in cecum graft tumor tissues. Moreover, the water and fodder consumption were significantly improved by MIF siRNA treatment. Importantly, MIF siRNA reduced the hepatic metastases from colorectal cancer. Our results suggest that siRNA targeting MIF is a promising agent for the treatment of hepatic metastasis of colorectal cancer cells.
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http://dx.doi.org/10.2741/4549 | DOI Listing |
Breast Cancer (Auckl)
September 2024
Research Center for Molecular Medicine, Institute of Cancer, Avicenna Health Research Institute (AHRI), Hamadan University of Medical Sciences, Hamadan, Iran.
As a heterogeneous disease, breast cancer (BC) has been characterized by the uncontrolled proliferation of mammary epithelial cells. The tumor microenvironment (TME) also contains inflammatory cells, fibroblasts, the extracellular matrix (ECM), and soluble factors that all promote BC progression. In this sense, the macrophage migration inhibitory factor (MIF), a pleiotropic pro-inflammatory cytokine and an upstream regulator of the immune response, enhances breast tumorigenesis through escalating cancer cell proliferation, survival, angiogenesis, invasion, metastasis, and stemness, which then brings tumorigenic effects by activating key oncogenic signaling pathways and inducing immunosuppression.
View Article and Find Full Text PDFJ Transl Med
July 2024
Department of Emergency, The Eighth Affiliated Hospital of Sun Yat- sen University, Shenzhen, 518003, Guangdong, P. R. China.
Introduction: Hepatocellular carcinoma (HCC) is characterized by the complex pathogenesis, limited therapeutic methods, and poor prognosis. Endoplasmic reticulum stress (ERS) plays an important role in the development of HCC, therefore, we still need further study of molecular mechanism of HCC and ERS for early diagnosis and promising treatment targets.
Method: The GEO datasets (GSE25097, GSE62232, and GSE65372) were integrated to identify differentially expressed genes related to HCC (ERSRGs).
Transl Cancer Res
June 2024
Department of Gastric Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.
Background: Prognosis of gastric cancer (GC) patients with ovarian metastasis (OM) remains poor. We hereby characterized the role of tumor immune microenvironment (TIME) and identified potential key regulators in the OM with the aim of understanding its molecular basis to develop novel therapeutic targets.
Methods: Transcriptomic analyses of paired primary and ovarian metastatic lesions of seven GC patients from Fudan University Shanghai Cancer Center uncovered and functionally annotated their differentially expressed genes (DEGs).
ACS Appl Mater Interfaces
January 2024
Department of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu 610041, China.
RNA interference-based gene therapy has led to a strategy for spinal cord injury (SCI) therapy. However, there have been high requirements regarding the optimal gene delivery vector for siRNA-based SCI gene therapy. Here, we developed an injectable and photocurable lipid nanoparticle GelMA (PLNG) hydrogel scaffold for controlled dual siRNA delivery at the SCI wound site.
View Article and Find Full Text PDFExp Eye Res
November 2023
Department of Cornea and Refractive Surgery, Aravind Eye Hospital, Madurai, India.
Therapeutic management of inflammation in infectious keratitis (IK) requires new strategy and targets for selective immunomodulation. Targeting host cell-type specific inflammatory responses might be a viable strategy to curtail unnecessary inflammation and reduce tissue damage without affecting pathogen clearance. This study explores the possibility of pathogen and host cell-type dependent differences in the inflammatory pathways relevant in the pathogenesis of IK.
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