Positive Mediators of Cell Proliferation in Neoplastic Transformation

Author(s):  
James N. Welch ◽  
Susan A. Chrysogelos
2020 ◽  
Vol 26 ◽  
Author(s):  
Yuying Qi ◽  
Chaoying Song ◽  
Jiali Zhang ◽  
Chong Guo ◽  
Chengfu Yuan

Background: Long non-coding RNA (LncRNAs), with the length over 200 nucleotides, originate from intergenic, antisense, or promoter-proximal regions, is a large family of RNAs that lack coding capacity. Emerging evidences illustrated that LncRNAs played significant roles in a variety of cellular functions and biological processes in profuse human diseases, especially in cancers. Cancer susceptibility candidate 9 (CASC9), as a member of the LncRNAs group, was firstly found its oncogenic function in esophageal cancer. In following recent studies, a growing amount of human malignancies are verified to be correlated with CASC9, most of which are derived from the squamous epithelium tissue. This present review attempts to highlight the latest insights into the expression, functional roles, and molecular mechanisms of CASC9 in different human malignancies. Methods: In this review, the latest findings related to the pathophysiological processes of CASC9 in human cancers were summarized and analyzed, the associated studies were collected in systematically retrieval of PubMed used lncRNA and CASA9 as keywords. Results: CASC9 expression is identified to be aberrantly elevated in a variety of malignancies. The over-expression of CASC9 has been suggested to accelerate cell proliferation, migration, cell growth and drug resistance of cancer cells, while depress cell apoptosis, revealing its role as an oncogene. Moreover, the current review demonstrated CASC9 closely relates to neoplastic transformation of squamous epithelial cells and squamous metaplasia in non-squamous epithelial tissues. Finally, we discuss the limitations and tremendous diagnostic/therapeutic potential of CASC9 in various human cancers. Results: CASC9 expression is identified to be aberrantly elevated in a variety of malignancies. The over-expression of CASC9 has been suggested to accelerate cell proliferation, migration, cell growth and drug resistance of cancer cells, while depress cell apoptosis, revealing its role as an oncogene. Moreover, the current review demonstrated CASC9 closely relates to neoplastic transformation of squamous epithelial cells and squamous metaplasia in non-squamous epithelial tissues. Finally, we discuss the limitations and tremendous diagnostic/therapeutic potential of CASC9 in various human cancers. Conclusion: Long non-coding RNACASC9 likely served as useful disease biomarkers or therapy targets that could effectively apply in treatment of different kinds of cancers.


2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Sara Baldelli ◽  
Dolores Limongi ◽  
Cristiana Coni ◽  
Fabio Ciccarone ◽  
Marco Ciotti ◽  
...  

Objectives. Some DNA viruses, such as BKPyV, are capable of inducing neoplastic transformation in human tissues through still unclear mechanisms. The goal of this study is to investigate the carcinogenic potential of BK polyomavirus (BKPyV) in human embryonic kidney 293 (Hek293) cells, dissecting the molecular mechanism that determines the neoplastic transformation. Materials and Methods. BKPyV, isolated from urine samples of infected patients, was used to infect monolayers of Hek293 cells. Subsequently, intracellular redox changes, GSH/GSSH concentration by HPLC, and reactive oxygen/nitrogen species (ROS/RNS) production were monitored. Moreover, to understand the signaling pathway underlying the neoplastic transformation, the redox-sensitive HFS1-Hsp27 molecular axis was examined using the flavonoid quercetin and polishort hairpin RNA technologies. Results. The data obtained show that while BKPyV replication is closely linked to the transcription factor p53, the increase in Hek293 cell proliferation is due to the activation of the signaling pathway mediated by HSF1-Hsp27. In fact, its inhibition blocks viral replication and cell growth, respectively. Conclusions. The HSF1-Hsp27 signaling pathway is involved in BKPyV infection and cellular replication and its activation, which could be involved in cell transformation.


Author(s):  
Ozal Arzuman A. Beylerli ◽  
Ilgiz F. Gareev ◽  
Adel Izmailov ◽  
Oleg N. Lipatov

With rapid advances in high-performance genome analysis technology, studying of long non-coding RNAs (lncRNAs) has become a very popular topic in biomedical research. LncRNAs are a group of non-coding RNAs with a length of more than 200 nucleotides. LncRNAs play a fundamental role in cell proliferation and differentiation, and epigenetic regulation. Thus, studying lncRNAs will give a new understanding of gene regulation and will open up new possibilities for treating and diagnosing many diseases, including tumors. The identification of new molecular markers in the form of circulating lncRNAs will improve tumor detection, predicting the course of the disease, treatment planning, and diagnosing at the earliest signs of upcoming neoplastic transformation. Treatment of tumors, especially malignant ones, is also a difficult task. When surgery and chemotherapy are not effective, radiation therapy becomes the treatment of choice. Therefore, the possibility of lncRNAs being innovative therapeutic agents in tumors is a viable idea. However, the possibility of their use in modern clinical practice is limited due to the number of problems associated with significant differences between procedures for processing samples, methods of analysis, and especially strategies for standardizing results. Another problem for conducting studies on the profiling of lncRNAs expression is their large number and the diversity of their functions in tumors. Therefore, the solution of technological problems on the profiling of lncRNAs expression in tumors may open up new possibilities for the use of lncRNAs in modern clinical practice.


1985 ◽  
Vol 5 (3) ◽  
pp. 538-544 ◽  
Author(s):  
S Alema ◽  
F Tato ◽  
D Boettiger

The effects of the avian viral oncogenes src and myc were compared for their ability to alter the differentiated phenotype and the proliferative capacity of definitive chondroblasts. As previously demonstrated, viruses carrying the src oncogene suppressed the synthesis of the chondroblast-specific products, type II collagen and cartilage-specific sulfated proteoglycan. In contrast, infection with MC29 and HB1 viruses, which carry the myc oncogene, did not suppress the synthesis of these normal differentiated cell products, but the infected cells exhibited an increased proliferative potential. The MH2 virus, which carries both the myc and mil oncogenes, both induced the suppression of these chondroblast-specific products and increased cell proliferation. The implications of these results for cooperation between oncogenes and the multi-oncogene models for neoplastic transformation are discussed.


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