Expression of TNF-related apoptosis inducing ligand receptors in different types of human cancer

Author(s):  
Anna Szumera-Cieckiewicz
2009 ◽  
Vol 5 (2) ◽  
pp. 125-131 ◽  
Author(s):  
Jin Song ◽  
Xiaer Sun ◽  
Lori J. Sokoll ◽  
Masatoshi Maki ◽  
Yuan Tian ◽  
...  

2020 ◽  
Vol 9 (1) ◽  
pp. 3-13
Author(s):  
Nguyen Hoang Danh ◽  
Thieu Hong Hue ◽  
Quang Trong Minh ◽  
K' Trong Nghia ◽  
Nguyen Thanh Tung ◽  
...  

miRNA (microRNA) are short RNA molecules in length from 20 to 24 nucleotides that have been shown to play an important role in regulating gene expression in many different types of human cancer. Meanwhile, miRNA-214 is one of the known miRNAs involved in the formation of nasopharyngeal carcinoma (NPC) through overexpression that promotes proliferation and development of cancer cells. However, in Vietnam, the study of miR-214 related to NPC has not been conducted yet. With the aims to develop the further studies of miR-214 on NPC in Vietnamese patients, in this initial study, we conducted the analysis of miR-214 expression in previous publications, as well as the prediction of miR-214 potential target genes, which involved in many cellular pathways. Here we applied bioinformatics tools to predict miRNAs and their targets, and discuss the role of miR-214 in the context of human cancers. As the results, miR-214 acted as the oncogenic roles in NPC, relevanted to many pathways, such as cell proliferation, apoptosis, metastasis and invasion through the its target genes LTF, Bim, Bax, LINC0086, etc. In conclusion, the use of computional approaches facilitate the further experimental validation of miRNAs in general, particularly miR-214, in Vietnamese NPC patients.


2020 ◽  
Vol 10 (6-s) ◽  
pp. 183-185
Author(s):  
Rajashri Champanery ◽  
Drashti Joshi

The tumor suppressor TP53 gene is one of the most frequently mutated in different types of human cancer. Particularly in colorectal cancer (CRC), it is believed that TP53 mutations play a role in the adenoma-carcinoma transition of tumors during pathological process. The TP53 mutation is the key step driving the transition from adenoma to adenocarcinoma. The functional roles of TP53 mutation in tumor development have been comprehensively investigated. In this mini review, we comprehensively summarize the p53 mutants in CRC progression and discuss the current strategies for p53 mutants in malignancies. Keywords: p53 mutants, colorectal cancer, Tp53 mutation


PPAR Research ◽  
2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Valerio Pazienza ◽  
Manlio Vinciguerra ◽  
Gianluigi Mazzoccoli

Nowadays, the study of the peroxisome proliferators activated receptors (PPARs) as potential targets for cancer prevention and therapy has gained a strong interest. From a biological point of view, the overall responsibility of PPARs in cancer development and progression is still controversial since several studies report both antiproliferative and tumor-promoting actions for these signaling molecules in human cancer cells and animal models. In this paper, we discuss PPARs functions in the context of different types of gastrointestinal cancer.


2021 ◽  
Vol 17 (8) ◽  
pp. 1510-1524
Author(s):  
Jian Zhou ◽  
Miao Lei ◽  
Xue-Liang Peng ◽  
Dai-Xu Wei ◽  
Lu-Ke Yan

Fenton reaction, a typical inorganic reaction, is broadly utilized in the field of wastewater treatment. Recently In case of its ability to inhibit the growth of cancer cells, it has been frequently reported in cancer treatment. Using the unique tumor microenvironment in cancer cells, many iron-based nanoparticles have been developed to release iron ions in cancer cells to induce Fenton reaction. In this mini review, we outline several different types of iron-based nanoparticles and several main means to enhance Fenton reaction in cancer cells. Finally, we discussed the advantages and disadvantages of iron-based nanoparticles for cancer therapy, prospected the future development of iron-based nanoparticles. It is believed that iron-based nanoparticles can make certain contribution to the cause of human cancer in the future.


2017 ◽  
Author(s):  
Jason T. Serviss ◽  
Felix Clemens Richter ◽  
Jimmy Van den Eynden ◽  
Nathanael Andrews ◽  
Miranda Houtman ◽  
...  

AbstractThe microRNA-34a is a well-studied tumor suppressor microRNA (miRNA) and a direct downstream target of TP53 with roles in several pathways associated with oncogenesis, such as proliferation, cellular growth, and differentiation. Due to its broad tumor suppressive activity, it is not surprising that miR34a expression is altered in a wide variety of solid tumors and hematological malignancies. However, the mechanisms by which miR34a is regulated in these cancers is largely unknown. In this study, we find that a long non-coding RNA transcribed antisense to the miR34a host gene, is critical for miR34a expression and mediation of its cellular functions in multiple types of human cancer. We name this long non-coding RNA lncTAM34a, and characterize its ability to facilitate miR34a expression under different types of cellular stress in both TP53 deficient and wild type settings.


Cancers ◽  
2018 ◽  
Vol 11 (1) ◽  
pp. 7 ◽  
Author(s):  
Ning Wang ◽  
Hor-Yue Tan ◽  
Yi-Gang Feng ◽  
Cheng Zhang ◽  
Feiyu Chen ◽  
...  

microRNA-23a (miR-23a) is one of the most extensively studied miRNAs in different types of human cancer, and plays various roles in the initiation, progression, and treatment of tumors. Here, we comprehensively summarize and discuss the recent findings about the role of miR-23a in cancer. The differential expression of tissue miR-23a was reported, potentially indicating cancer stages, angiogenesis, and metastasis. miR-23a in human biofluid, such as plasma and salivary fluid, may be a sensitive and specific marker for early diagnosis of cancer. Tissue and circulating miR-23a serves as a prognostic factor for cancer patient survival, as well as a predictive factor for response to anti-tumor treatment. The direct and indirect regulation of miR-23a on multiple gene expression and signaling transduction mediates carcinogenesis, tumor proliferation, survival, cell migration and invasion, as well as the response to anti-tumor treatment. Tumor cell-derived miR-23a regulates the microenvironment of human cancer through manipulating both immune function and tumor vascular development. Several transcriptional and epigenetic factors may contribute to the dysregulation of miR-23a in cancer. This evidence highlights the essential role of miR-23a in the application of cancer diagnosis, prognosis, and treatment.


2021 ◽  
Vol 22 (14) ◽  
pp. 7369
Author(s):  
Carlos Jhovani Pérez-Amado ◽  
Amellalli Bazan-Cordoba ◽  
Alfredo Hidalgo-Miranda ◽  
Silvia Jiménez-Morales

Cancer is a serious health problem with a high mortality rate worldwide. Given the relevance of mitochondria in numerous physiological and pathological mechanisms, such as adenosine triphosphate (ATP) synthesis, apoptosis, metabolism, cancer progression and drug resistance, mitochondrial genome (mtDNA) analysis has become of great interest in the study of human diseases, including cancer. To date, a high number of variants and mutations have been identified in different types of tumors, which coexist with normal alleles, a phenomenon named heteroplasmy. This mechanism is considered an intermediate state between the fixation or elimination of the acquired mutations. It is suggested that mutations, which confer adaptive advantages to tumor growth and invasion, are enriched in malignant cells. Notably, many recent studies have reported a heteroplasmy-shifting phenomenon as a potential shaper in tumor progression and treatment response, and we suggest that each cancer type also has a unique mitochondrial heteroplasmy-shifting profile. So far, a plethora of data evidencing correlations among heteroplasmy and cancer-related phenotypes are available, but still, not authentic demonstrations, and whether the heteroplasmy or the variation in mtDNA copy number (mtCNV) in cancer are cause or consequence remained unknown. Further studies are needed to support these findings and decipher their clinical implications and impact in the field of drug discovery aimed at treating human cancer.


2021 ◽  
Author(s):  
Shouping Xu ◽  
Lin Wan ◽  
Qin Wang ◽  
Huizi Yin ◽  
Kun Qiao ◽  
...  

Abstract Background: The oncogenic lncRNA based strategies for combating cancer may usher in a new and promising paradigm in cancer therapy. However, few studies have been performed to solve such a critical issue. The complex traits and molecular mechanism of such lncRNAs in tumorigenesis and their relationship with sensitivity of gefitinib in human cancer have not been investigated.Methods: We aimed to identify and validate such a novel oncogenic LINC00036 using transcriptome sequencing approach and a large number of tissue samples of different types of cancer from the our cancer center cohort and public data cohorts from the Cancer Genome Atlas,Gene Expression Omnibus and Cancer Cell Line Encyclopedia. Moreover, series of in vitro and in vivo experiments were performed to examine its roles in tumorigenesis and the sensitivity of gefitinib in different types of cancer cells. Special nanoparticle via a more potent delivery system was developed to investigate the feasibility of targeting LINC00036 in vivo. Furthermore, chromatin immunoprecipitation (ChIP)-sequencing, ChIP, actinomycin D assay, dual-luciferase reporter assay, RNA pull-down and RNA immunoprecipitation were performed were developed to uncover the molecular mechanism.Results: LINC00036 that associated with poor prognosis is significantly upregulated in human cancer tissues. Series of in vitro and in vivo experiments reveal that LINC00036 promotes tumorigenesis and decreases the sensitivity of gefitinib in different types of cancer cells. LINC00036 targeting nanoparticle markedly reduced the growth of human cancer xenografts. Mechanistically, LINC00036 is a direct transcriptional target of c-MYC and a positive feedback loop of the c-MYC-LINC00036-EGFR axis exists in human cancer. LINC00036 acts as an EGFR mRNA stabilizer via RNA-protein and RNA-RNA interactions, inducing the hyper-activation of the downstream AKT and MAPK signaling pathways, which in turn decreases the sensitivity of gefitinib in human cancer.Conclusions: LINC00036, a c-MYC inducible onco-lncRNA, acts an oncogene in human cancer and decreases the sensitivity of gefitinib through positive feedback loop of the c-MYC-LINC00036-EGFR axis. Overall, this study broadens knowledge regarding novel onco-lncRNAs and will assist in developing feasible onco-lncRNAs based-targeted therapeutic strategies to improve the sensitivity of gefitinib in human cancer.


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