Abstract
Malignant pleural mesothelioma (MPM) is a rare malignancy, with extremely poor survival rates. At present, treatment options are limited, with no second line chemotherapy for those who fail first line therapy. Extensive efforts are ongoing in a bid to characterise the underlying molecular mechanisms of mesothelioma. Recent research has determined that between 70–90% of our genome is transcribed. As only 2% of our genome is protein coding, the roles of the remaining proportion of non-coding RNA in biological processes has many applications, including roles in carcinogenesis and epithelial–mesenchymal transition (EMT), a process thought to play important roles in MPM pathogenesis. Non-coding RNAs can be separated loosely into two subtypes, short non-coding RNAs (<200 nucleotides) or long (>200 nucleotides). A significant body of evidence has emerged for the roles of short non-coding RNAs in MPM. Less is known about the roles of long non-coding RNAs (lncRNAs) in this disease setting. LncRNAs have been shown to play diverse roles in EMT, and it has been suggested that EMT may play a role in the aggressiveness of MPM histological subsets. In this report, using both in vitro analyses on mesothelioma patient material and in silico analyses of existing RNA datasets, we posit that various lncRNAs may play important roles in EMT within MPM, and we review the current literature regarding these lncRNAs with respect to both EMT and MPM.
Highlights
Malignant pleural mesothelioma (MPM) is a rare, but aggressive form of cancer, predominantly associated with prior exposure to asbestos [1]
The epithelioid and sarcomatoid histologic variants of MPM can be considered as E- and M-parts of the Epithelial–mesenchymal transition (EMT) axis, with the biphasic histotype considered an intermediate [14]
We examined the expression of a novel series of long non-coding RNAs (lncRNAs) (Epidermal Growth Factor Receptor- antisense RNA 1 EGFR-AS1, prostate cancer associated transcript 6 PCAT6 and zinc finger E-box binding homeobox 2 antisense RNA 1 ZEB2-AS1) for altered expression in MPM
Summary
Malignant pleural mesothelioma (MPM) is a rare, but aggressive form of cancer, predominantly associated with prior exposure to asbestos [1]. A recent report based on extrapolations for asbestos use estimated global mesothelioma deaths at 38,400 per annum [3], and while there have been some recent advances in this disease, with respect to immune-oncology [4,5], the current standard of care (a combination of pemetrexed/raltitrexed and cisplatin chemotherapy) [6,7] is non-curative, and results in a response rate of approximately 40% [8]. Epithelial–mesenchymal transition (EMT) is a process by which epithelial cells shed many of their epithelial traits and acquire various features observed in mesenchymal cells. During this transition, epithelial cells lose their polarity and many of their intercellular contacts, such as desmosomes, adherens junctions, and tight junctions, resulting in their disassociation from epithelial sheets. At the end of this process, cells undergoing EMT assume a variety of mesenchymal-like properties: enhanced migratory capacity, invasiveness, heightened resistance to apoptosis, and greatly increased production of extracellular matrix components [9]
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