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Thus the loss of ATP-dependence of RNA release observed earlier in several non-neural cell-types after exposure to carcinogens, or after neoplastic transformation, is not an essential attribute of the carcinogenic process.
Its inhibition may thus be carcinogenic.
Bulk RNAseq of environmentally-induced mouse tumors can reveal carcinogenic exposures and causes.
It is suggested that UV-induced disruption of miRNA-mediated gene regulation plays a carcinogenic role.
Small interfering RNA (siRNA) has the ability to knock down the expression of carcinogenic genes or drug efflux transporter genes, paving the way for cancer treatment.
We hypothesize that lncRNAs have potential as epigenetic biomarkers of carcinogenic exposures.
Gene ontology analysis indicated that most commonly-altered mRNAs participate in carcinogenic steps.
Thus, alterations in methylation contribute directly to the carcinogenic potential of the cells.
It is proposed that alterations of minor nucleotides in the maturation of tRNA could be basic to the carcinogenic process.
It is indicated that RNAi application for targeting functional carcinogenic molecules, tumor resistance to chemotherapy and radiotherapy is required in cancer treatment.

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