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1.
Front Immunol ; 12: 781032, 2021.
Article in English | MEDLINE | ID: mdl-34858438

ABSTRACT

The activation of stimulator of interferon genes (STING) signalling pathway has been suggested to promote the immune responses against malignancy. STING is activated in response to the detection of cytosolic DNA and can induce type I interferons and link innate immunity with the adaptive immune system. Due to accretive evidence demonstrating that the STING pathway regulates the immune cells of the tumor microenvironment (TME), STING as a cancer biotherapy has attracted considerable attention. Pancreatic cancer, with a highly immunosuppressive TME, remains fatal cancer. STING has been applied to the treatment of pancreatic cancer through distinct strategies. This review reveals the role of STING signalling on pancreatic tumors and other diseases related to the pancreas. We then discuss new advances of STING in either monotherapy or combination methods for pancreatic cancer immunotherapy.


Subject(s)
Immunotherapy/methods , Membrane Proteins/immunology , Nucleotidyltransferases/immunology , Pancreatic Neoplasms/immunology , Pancreatic Neoplasms/therapy , Humans , Signal Transduction/immunology
2.
Front Cell Dev Biol ; 9: 737670, 2021.
Article in English | MEDLINE | ID: mdl-34692695

ABSTRACT

Long non-coding RNAs (lncRNAs) are a type of non-coding RNAs that act as molecular fingerprints and modulators of many pathophysiological processes, particularly in cancer. Specifically, lncRNAs can be involved in the pathogenesis and progression of brain tumors, affecting stemness/differentiation, replication, invasion, survival, DNA damage response, and chromatin dynamics. Furthermore, the aberrations in the expressions of these transcripts can promote treatment resistance, leading to tumor recurrence. The development of next-generation sequencing technologies and the creation of lncRNA-specific microarrays have boosted the study of lncRNA etiology. Cerebrospinal fluid (CSF) directly mirrors the biological fluid of biochemical processes in the brain. It can be enriched for small molecules, peptides, or proteins released by the neurons of the central nervous system (CNS) or immune cells. Therefore, strategies that identify and target CSF lncRNAs may be attractive as early diagnostic and therapeutic options. In this review, we have reviewed the studies on CSF lncRNAs in the context of brain tumor pathogenesis and progression and discuss their potential as biomarkers and therapeutic targets.

3.
Front Oncol ; 10: 515421, 2020.
Article in English | MEDLINE | ID: mdl-33194577

ABSTRACT

Deregulations of long non-coding RNAs (lncRNAs) have been implicated in the progression of breast cancer (BC). However, the prognostic values of those lncRNAs in BC remain elusive. This study aimed at constructing a lncRNA-based prognostic model to improve the clinical management of BC. Systematic investigation of lncRNA expression profiles and clinical data from The Cancer Genome Atlas (TCGA) database were utilized to establish a 10-lncRNA signature. The prognostic signature efficiently discriminated patients with significantly different prognosis regardless of intrinsic molecular subtypes and tumor-node-metastasis (TNM) stage. A combined model was constructed by multivariate Cox proportional hazards regression (CPHR) analysis, which combined the lncRNA-based signature with certain clinical risk factors (TNM stage, age, and human epidermal growth factor receptor 2 status). This model predicted a survival probability that closely corresponds to the actual survival probability. With respect to the entire set, the time-dependent receiver-operating characteristic curves revealed that the area under the curve of this model was the highest than any of the clinical risk factors. Moreover, functional enrichment analysis indicated that the molecular signature was mainly involved in DNA replication, which was firmly related to BC tumorigenesis. Consistent with the discovery, the knockdown of LHX1-DT, one of the 10 prognostic lncRNAs, attenuated the proliferation of BC cells in vitro and in vivo. Taken together, our study constructed a novel 10-lncRNA signature for prediction prognosis, and the signature-based model could provide new insight into accurate management of BC patients.

4.
Mol Cancer ; 19(1): 132, 2020 08 27.
Article in English | MEDLINE | ID: mdl-32854710

ABSTRACT

At the moment, pancreatic cancer is among the deadliest gastrointestinal diseases, and pancreatic cancer growth is a complex biological process that is based on different kinds of genes. Exosomes are extracellular vesicles containing microRNAs (miRNAs), messenger RNA (mRNA), and proteins, they act as the most prominent mediator of intercellular communication, and they regulate, instruct, and re-educate their surrounding microenvironment and target specific organs. Due to accumulative evidence proved that exosomes are involved in metastasis, cell proliferation, EMT, angiogenesis, and TME of pancreatic cancer, exosomes are crucial potential candidates to detect pancreatic cancer early. This review aims to convey the current understanding of the main functions employed by exosomes in early diagnosis and treatment of pancreatic cancer.


Subject(s)
Biomarkers, Tumor/genetics , MicroRNAs/genetics , Pancreatic Neoplasms/diagnosis , RNA, Messenger/genetics , Cell Proliferation/genetics , Exosomes/genetics , Extracellular Vesicles/genetics , Gene Expression Regulation, Neoplastic/genetics , Humans , Pancreatic Neoplasms/genetics , Pancreatic Neoplasms/pathology , Tumor Microenvironment/genetics , Pancreatic Neoplasms
5.
Pancreatology ; 20(1): 79-88, 2020 Jan.
Article in English | MEDLINE | ID: mdl-31780287

ABSTRACT

Pancreatic ductal adenocarcinoma (PDAC) is among the dangerous human cancers, is the 10th highly prevalent cancer, and the fourth sole cause of cancer-related mortality in the United States of America. Notwithstanding the significant commitment, the forecast for people with this burden continues to have a five-year survival rate of just 4-6%. The most critical altered genes within PDAC consist of K-ras the proto-oncogene which is usually mutationally activated above 90% cases and tumor suppressors likeTrp53 are altered at 55%. To face the burden of pancreatic ductal adenocarcinoma, a variety of genetically engineered pancreatic cancer mice models have been created over the last past years. These models have distinctive features and are not all appropriate for preclinical studies. In this review, we focus on differences between two mice models K-rasLSL.G12D/+;Pdx-1-Cre(KC) and K-rasLSL.G12D/+; Trp53R172H/+; Pdx-1-Cre(KPC) in terms of their modeling biology and their clinical relevance.


Subject(s)
Carcinoma, Pancreatic Ductal/genetics , Disease Models, Animal , Pancreatic Neoplasms/genetics , Animals , Genetic Predisposition to Disease , Mice , Mice, Inbred Strains , Mutation , Proto-Oncogene Mas
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