scholarly journals Diagnostic role of gastrin-releasing peptide receptors in oncology

2021 ◽  
Vol 12 (1) ◽  
pp. 21-34
Author(s):  
P. Korol ◽  
O. Shcherbina
Keyword(s):  
Cancer Cells ◽  
High Sensitivity ◽  
Biological Behavior ◽  
Peptide Receptors ◽  
Primary Tumors ◽  
Gastrin Releasing Peptide ◽  
Metastatic Lesions ◽  
Diagnostic Role ◽  
Theranostic Agents

Tumor receptor-targeted diagnostic imaging is an area of research that identifies a biomarker that is overexpressed on the surface of cancer cells and binds its ligand to carriers, allowing imaging of the tumor process. The success of this approach depends on the selectivity of the receptor for certain malignant cells, as well as on its ability to specifically bind to the target ligand. This review examines the diagnostic role of the bombesin family of receptors, which focus on gastrin-releasing peptide receptors (GRPR), which are overexpressed in various cancers. For tumors expressing GRPR, the diagnostic informativeness of the detection of both primary tumor foci and metastases is high. The well-known concept of tumor heterogeneity has led to the development of bivalent prostate cancer - target peptides with the ability to target two receptors. Radiolabeled bombesin analogues are promising theranostic agents for tumors that express GRPR, which opens the possibility of early detection of primary tumors and metastatic lesions with high sensitivity and specificity. At the same time, further forward-looking clinical trials are needed to improve understanding of the relationship between GRPR expression and the biological behavior of different cancer cells. Key words: gastrin-releasing peptide receptors, bombesin, theranostic, oncology

Targeting gastrin-releasing peptide receptors of prostate cancer cells for photodynamic therapy with a phthalocyanine–bombesin conjugate

2008 ◽  
Vol 18 (7) ◽  
pp. 2424-2427 ◽  
Author(s):  
Céléna Dubuc ◽  
Réjean Langlois ◽  
François Bénard ◽  
Nicole Cauchon ◽  
Klaus Klarskov ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Photodynamic Therapy ◽  
Cancer Cells ◽  
Prostate Cancer Cells ◽  
Peptide Receptors ◽  
Gastrin Releasing Peptide

scholarly journals Identification of microRNA-451a as a Novel Circulating Biomarker for Colorectal Cancer Diagnosis

2020 ◽  
Vol 2020 ◽  
pp. 1-18
Author(s):  
Zhen Zhang ◽  
Dai Zhang ◽  
Yaping Cui ◽  
Yongsheng Qiu ◽  
Changhong Miao ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Diagnosis ◽  
Potential Role ◽  
High Sensitivity ◽  
Primary Tumors ◽  
Circulating Biomarker ◽  
Microarray Profiling ◽  
Downstream Analysis ◽  
Microrna Microarray

Background. Colorectal cancer (CRC) is one of the leading causes of cancer death worldwide. Successful treatment of CRC relies on accurate early diagnosis, which is currently a challenge due to its complexity and personalized pathologies. Thus, novel molecular biomarkers are needed for early CRC detection. Methods. Gene and microRNA microarray profiling of CRC tissues and miRNA-seq data were analyzed. Candidate microRNA biomarkers were predicted using both CRC-specific network and miRNA-BD tool. Validation analyses were carried out to interrogate the identified candidate CRC biomarkers. Results. We identified miR-451a as a potential early CRC biomarker circulating in patient’s serum. The dysregulation of miR-451a was revealed both in primary tumors and in patients’ sera. Downstream analysis validated the tumor suppressor role of miR-451a and high sensitivity of miR-451a in CRC patients, further confirming its potential role as CRC circulation biomarker. Conclusion. The miR-451a is a potential circulating biomarker for early CRC diagnosis.

scholarly journals A novel protein encoded by circMAPK1 inhibits progression of gastric cancer by suppressing activation of MAPK signaling

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Tianlu Jiang ◽  
Yiwen Xia ◽  
Jialun Lv ◽  
Bowen Li ◽  
Ying Li ◽  
...  
Keyword(s):  
Mass Spectrometry ◽  
Gastric Cancer ◽  
Cancer Cells ◽  
Mapk Pathway ◽  
Biological Behavior ◽  
Gastric Cancer Cells ◽  
Novel Protein

Abstract Background A novel type of noncoding RNA, circRNA has been reported to participate in the occurrence and development of diseases through many mechanisms. The MAPK pathway is a common signal transduction pathway involved in cell proliferation, inflammation and apoptosis and plays a particularly important role in cancers. However, the role of circRNAs related to the MAPK pathway in gastric cancer has not been explored. Methods A bioinformatics analysis was performed to profile and identify the circRNAs involved in the MAPK pathway in gastric cancer. The tumor-suppressive role of circMAPK1 was confirmed both in vitro and in vivo. Mass spectrometry, Western blot and immunofluorescence staining assays were used to validate the existence and expression of MAPK1–109aa. The molecular mechanism of circMAPK1 was investigated by mass spectrometry and immunoprecipitation analyses. Results In this study, we identified that circMAPK1 (hsa_circ_0004872) was downregulated in gastric cancer tissues compared with adjacent normal tissues. Importantly, lower circMAPK1 expression predicted poor survival in GC patients. CircMAPK1 inhibited the proliferation and invasion of gastric cancer cells in vitro and in vivo. Next, we found that circMAPK1 encoded a novel protein with 109 amino acids in length. Through a series of functional experiments, we confirmed that circMAPK1 exerted a tumor-suppressing effect via the encoded protein MAPK1–109aa. Mechanistically, the tumor suppressor MAPK1–109aa inhibited the phosphorylation of MAPK1 by competitively binding to MEK1, thereby suppressing the activation of MAPK1 and its downstream factors in MAPK pathway. Conclusions Our study revealed that circMAPK1 inhibits the malignant biological behavior of gastric cancer cells through its encoded protein MAPK1–109aa. More importantly, circMAPK1 is a favorable predictor for gastric cancer patients and may provide a new therapeutic target in the treatment of gastric cancer.

scholarly journals AGER promotes proliferation and migration in cervical cancer

2018 ◽  
Vol 38 (1) ◽  
Author(s):  
Xuejie Zhu ◽  
Lulu Zhou ◽  
Ruyi Li ◽  
Qi Shen ◽  
Huihui Cheng ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Tumor Promoter ◽  
Biological Behavior ◽  
Squamous Cervical Cancer ◽  
Glycation End Products ◽  
Squamous Cancer ◽  
And Migration ◽  
Cervical Squamous Cancer

The receptor for advanced glycation end products (AGER) is an oncogenic transmembranous receptor up-regulated in various human cancers. We have previously reported that AGER was overexpressed in squamous cervical cancer. However, mechanisms of AGER involved in the progression of cervical cancer are unknown. In the present study, we investigated the effects of AGER on biological behavior, including proliferation, apoptosis, and migration using multiple biological approaches. AGER protein primarily localized in the cytoplasm and cytomembrane of cervical squamous cancer cells. Blockage of AGER with multiple siRNAs suppressed proliferation, stimulated apoptosis, inhibited migration of cervical squamous cancer cells. Conversely, overexpression of AGER increased cell proliferation, migration, and inhibited cell apoptosis. These results indicate that AGER promotes proliferation, migration, and inhibits apoptosis of squamous cervical cancer and might function as a tumor promoter in cervical cancer. Our study provides novel evidence for a potential role of AGER in bridging human papillomavirus (HPV)-induced inflammation and cervical cancer.

scholarly journals Remodeling the ECM: Implications for Metastasis and Tumor Dormancy

Cancers ◽  
2021 ◽  
Vol 13 (19) ◽  
pp. 4916
Author(s):  
Julie S. Di Martino ◽  
Tasmiah Akhter ◽  
Jose Javier Bravo-Cordero
Keyword(s):  
Cancer Cells ◽  
Tumor Cells ◽  
Cancer Progression ◽  
Current Knowledge ◽  
Disseminated Tumor Cells ◽  
Tumor Dormancy ◽  
Primary Tumors ◽  
Ecm Remodeling ◽  
The Individual

While most primary tumors can be effectively treated, therapeutics fail to efficiently eliminate metastases. Metastases arise from cancer cells that leave the primary tumor and seed distant sites. Recent studies have shown that cancer cells disseminate early during tumor progression and can remain dormant for years before they resume growth. In these metastatic organs, cancer cells reside in microenvironments where they interact with other cells, but also with the extracellular matrix (ECM). The ECM was long considered to be an inert, non-cellular component of tissues, providing their architecture. However, in recent years, a growing body of evidence has shown that the ECM is a key driver of cancer progression, and it can exert effects on tumor cells, regulating their metastatic fate. ECM remodeling and degradation is required for the early steps of the metastatic cascade: invasion, tumor intravasation, and extravasation. Similarly, ECM molecules have been shown to be important for metastatic outgrowth. However, the role of ECM molecules on tumor dormancy and their contribution to the dormancy-supportive niches is not well understood. In this perspective article, we will summarize the current knowledge of ECM and its role in tumor metastasis and dormancy. We will discuss how a better understanding of the individual components of the ECM niche and their roles mediating the dormant state of disseminated tumor cells (DTCs) will advance the development of new therapies to target dormant cells and prevent metastasis outgrowth.

scholarly journals Shedding Light on the Role of Neurotransmitters in the Microenvironment of Pancreatic Cancer

2021 ◽  
Vol 9 ◽  
Author(s):  
Yiyi Liang ◽  
Huimin Li ◽  
Yu Gan ◽  
Hong Tu
Keyword(s):  
Pancreatic Cancer ◽  
Immune Responses ◽  
Cancer Cells ◽  
Immune Cells ◽  
Stromal Cells ◽  
Biological Behavior ◽  
Adaptive Immune ◽  
Extracellular Matrix Components ◽  
Cellular Components

Pancreatic cancer (PC) is a highly lethal malignancy with a 5-year survival rate of less than 8%. The fate of PC is determined not only by the malignant behavior of the cancer cells, but also by the surrounding tumor microenvironment (TME), consisting of various cellular (cancer cells, immune cells, stromal cells, endothelial cells, and neurons) and non-cellular (cytokines, neurotransmitters, and extracellular matrix) components. The pancreatic TME has the unique characteristic of exhibiting increased neural density and altered microenvironmental concentration of neurotransmitters. The neurotransmitters, produced by both neuron and non-neuronal cells, can directly regulate the biological behavior of PC cells via binding to their corresponding receptors on tumor cells and activating the intracellular downstream signals. On the other hand, the neurotransmitters can also communicate with other cellular components such as the immune cells in the TME to promote cancer growth. In this review, we will summarize the pleiotropic effects of neurotransmitters on the initiation and progression of PC, and particularly discuss the emerging mechanisms of how neurotransmitters influence the innate and adaptive immune responses in the TME in an autocrine or paracrine manner. A better understanding of the interplay between neurotransmitters and the immune cells in the TME might facilitate the development of new effective therapies for PC.

scholarly journals Epigenetic Regulation by lncRNAs: An Overview Focused on UCA1 in Colorectal Cancer

Cancers ◽  
2018 ◽  
Vol 10 (11) ◽  
pp. 440 ◽  
Author(s):  
Bernadette Neve ◽  
Nicolas Jonckheere ◽  
Audrey Vincent ◽  
Isabelle Van Seuningen
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Cell Cycle Progression ◽  
Cycle Progression ◽  
Regulate Gene Expression ◽  
Metastatic Lesions ◽  
Colorectal Cancer Cells ◽  
Regulation Of Cell Cycle ◽  
Integrate Research

Colorectal cancers have become the second leading cause of cancer-related deaths. In particular, acquired chemoresistance and metastatic lesions occurring in colorectal cancer are a major challenge for chemotherapy treatment. Accumulating evidence shows that long non-coding (lncRNAs) are involved in the initiation, progression, and metastasis of cancer. We here discuss the epigenetic mechanisms through which lncRNAs regulate gene expression in cancer cells. In the second part of this review, we focus on the role of lncRNA Urothelial Cancer Associated 1 (UCA1) to integrate research in different types of cancer in order to decipher its putative function and mechanism of regulation in colorectal cancer cells. UCA1 is highly expressed in cancer cells and mediates transcriptional regulation on an epigenetic level through the interaction with chromatin modifiers, by direct regulation via chromatin looping and/or by sponging the action of a diversity of miRNAs. Furthermore, we discuss the role of UCA1 in the regulation of cell cycle progression and its relation to chemoresistance in colorectal cancer cells.

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