Paper 9: microRNA in non-melanoma skin cancer
MicroRNAs (miRNAs) are 17- to 23-nucleotide (nt), short, non-coding RNA molecules that are capable of regulating gene expression at a posttranscriptional level. Encoded within both exons and introns, they play a pivotal role in a variety of physiologic ce
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Paper 9: microRNA in non-melanoma skin cancer *
13.1 Introduction MicroRNAs (miRNAs) are 17- to 23-nucleotide (nt), short, non-coding RNA molecules that are capable of regulating gene expression at a posttranscriptional level. Encoded within both exons and introns, they play a pivotal role in a variety of physiologic cellular functions and diseases, including cancer. Approximately 30%–60% of all human genes are affected by miRNA regulation, and our understanding of their role as both tumor suppressors and oncogenes in a variety of different cancers is gradually evolving. In this mini-review, we summarize the current knowledge on the role of miRNAs in non-melanoma skin cancer (NMSC). All the differentially expressed miRNAs in NMSC have been compiled in table 12-1. 13.2 miRNA maturation and function Briefly, miRNA maturation begins in the nucleus where RNA polymerase II transcribes the primary-miRNA (pri-miRNA) transcript. Drosha, an intranuclear RNase III endonuclease, and its co-factor, DiGeorge syndrome critical region gene 8 (DGCR8 or Pasha (Partner of Drosha)), form the microprocessor complex that cleaves the pri-miRNA transcript into several 70–90-nt precursor-miRNAs (pre-miRNAs) that share a characteristic stem loop structure [1]. These pre-miRNAs are transported from the nucleus to the cytoplasm by exportin-5 (Exp-5). In the cytoplasm, Dicer, an extranuclear RNase III enzyme, cuts the premiRNAs into mature miRNA strands, that are loaded into the RNAinduced silencing complex (RISC). Depending on the degree of complementarity between the target mRNA and the miRNA, binding either stops translation by cleaving the target mRNA (full complementarity) or suppresses translation by binding to and impeding ribosomal reading of the mRNA (incomplete complementarity).
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Co-authors: Daniel Sand M.D., Peter Altmeyer M.D., Falk G. Bechara M.D.
© Springer Fachmedien Wiesbaden 2016 M. Sand, MicroRNAs in malignant tumors of the skin, DOI 10.1007/978-3-658-12794-7_13
Regulation
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+
+
+
+
+
miRNA
let-7
hsamiR-17
hsamiR18a
hsamiR18b
hsamiR19b
hsamiR19b-1*
BCC
BCC
BCC
BCC
BCC
BCC
Tumor
member of the hsa-miR-17-92 cluster, also known as Oncomir-1; responsible for enhanced cell proliferation and the suppression of apoptosis member of the hsa-miR-17-92 cluster, also known as Oncomir-1; responsible for enhanced cell proliferation and the suppression of apoptosis
pro-growth miRNA regulated in vitro by MAPK »ERK-induced phosphorylation of TRBP member of the hsa-miR-17-92 cluster, also known as Oncomir-1; responsible for enhanced cell proliferation and the suppression of apoptosis same seed sequence as hsa-miR-18a
involved in regulating cell proliferation
Molecular Impact
He et al.[30] Al-Nakhle et al.[31]
Sand et al.[13]
He et al.[30] Al-Nakhle et al.[31] He et al.[30] Al-Nakhle et al.[31]
Sand et al.[13]
Sand et al.[13]
Sand et al.[13]
Heffelfinger et al.[12] Parroo et al. [29]
Author Molecular Impact
Heffelfinger et al.[12] Sand et al.[13]
Author miRNA
234 13 Paper 9
Tab. 13-1: Listing selected
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