miR-24-2 regulates genes in survival pathway and demonstrates potential in reducing cellular viability in combination with docetaxel

• miR-24-2 target prediction identifies essential cell survival and stability genes.
• PPi identifies nodes regulating cell cycle and differential oncogenesis.
• Negative correlation between hsa-miR-24-2 and increasing nodes and metastasis.
• hsa-miR-24-2 targeting genes of cell survival correlate with methylation profile.
• Potential of hsa-miR-24-2 to reduce cellular viability in presence of docetaxel.

MicroRNAs the small (18–22 in length) noncoding RNA molecules are negative regulators of gene expression, modulating biological processes of cell differentiation, survival and death. The latter two phenomena are critical in tumour biology. We provide here the results of human genome wide target prediction of one such microRNA, hsa-miR-24-2, shown to target genes essential for initiating cellular stability and cell survival. The protein–protein interaction study showed important nodes which could affect cell cycle progression and differential oncogenesis. An analysis of hsa-miR-24-2 in sporadic breast tumours showed a negative correlation with metastasis and increasing nodes. The conclusion drawn of hsa-miR-24-2 targeting the genes of cell survival correlated with the methylation profile and resultant transcription factor binding site gain or loss in support of absence of cell survival. In order to accentuate the potential of hsa-miR-24-2 to reduce cellular viability under experimental conditions, in vitro studies in the presence and absence of anti-cancer drugs, such as docetaxel resulted in a significant decrease in cellular viability even at a 200-fold reduced dose of the drug in combination with hsa-miR-24-2.