Increase, Mutations leads to Increase,miRNA levels

In response to stressors like as ionising radiation, miRNAs are differently regulated. When exposed to IR, miRNA expression is frequently disrupted. Some miRNAs are induced by IR, while others are suppressed, a decision that is likely based on the target genes implicated. This figure summarises the miRNAs mentioned in this review whose expression changes in response to IR. Lists of miRNAs whose induction or repression has been detected are on the left and right, respectively. MiRNAs are in the middle, and both induction and repression have been found in many cell types. The centre contains the biggest group of miRNAs, demonstrating how diverse the miRNA profile can be from one cell type to the next. Bold miRNAs play a role in several parts of the DDR.

Induced miRNAs were reported by some studies (Cha et al.,2009;Chaudhary et al 201; Chaudhary et al 2012; Chaudhary et al 2013;Kwon et al.,2013;Mueller et al.,2013;Shin et al.,2009;Sokolov et al.,2012;Wagner et al.,2010),whereas repressed miRNAs are observed in some(Cha et al., 2009,Chaudhari et al.,2010).Both induction and repression of some miRNA were seen in different cell types and results are inconclusive (Cha et al.,2009;Chaudhary et al 201; Chaudhary et al 2012; Chaudhary et al 2013;Kwon et al.,2013;Mueller et al.,2013;Shin et al.,2009;Sokolov et al.,2012;Wagner et al.,2010; Kraemer et al., 2011; Moskwa et al.,2011;Niemoeller et al.,2011;Sokolov et al., 2012;Wagner et al.,2010).This inconsistency could be due to different doses of stressor.

DNA damage response influences miRNA expression, at the same time miRNA can also influence DDR, cell cycle etc.The miR-34 family produces a cell-cycle arrest in the G1 phase and slows cell-cycle progression by targeting multiple cell cycle regulators when ectopically produced, implying tumor-suppressing potential. The miR-34 family, for example, specifically targets and inhibits cyclin-dependent kinase 4 (CDK4), CDK6, E2F3, Myc, and NMYC (Chang  et al.,2007,He et al., 2007).

MiRNA expression can be influenced by DNA damage and mutation, but miRNA can also regulate DNA damage response and cell cycle.By suppressing the transcripts of numerous genes that govern cell-cycle checkpoints or metabolism, these p53-induced miRNAs contribute to cell-cycle arrest (Su et al.,2010;Georges et al.,2008;Hermeking et al.,2012;Klein et al., 2010; Liu et al.,2011; Suh et al.,2011). Wip1 phosphatase, a master inhibitor in the DDR that inhibits the activation and stability of p53, is targeted and repressed by miR-16 and miR-29, resulting in p53 induction (Ugalde et al.,2011; Zhang et al.,2010). Cellcycle arrest is induced by ectopic expression of miR-192/215, which targets a number of genes that regulate the G1/S and G2/M checkpoints (Bulavin et al.,2004).

The oncogene c-Myc is directly targeted by miR-145, implying that p53 suppresses cMyc activities through regulating miRNA expression (Sachdeva et al.,2009, Suh et al.,2011). p53-induced miRNAs, interestingly, influence p53 activity in a positive feedback loop (Han et al.,2012, Hermeking et al.,2012). SIRT1 acetylation and activation are increased when miR-34 inhibits it (Yamakuchi et al., 2008). Mdm2 expression is directly inhibited by miR-192, miR-194, miR-215, and MiR-605, while Wip1 is inhibited by miR-29, resulting in higher p53 levels and activity. (Braun et al.,2008, Pichiorri et al.,2010, Xiao et al., 2011).

Activity of pri-miR-218, pri-miR-16-1, pri-miR-21, and pri- miR-199a had significantly increased binding with Drosha (2.5- to 3.2-fold) after DNA damage (Zhang et al.,2011)

It has been noted that, within hours of DNA damage,miRNA expression were induced(Wan et al.,2013).

Not specific ones available.