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Background: The activation of peroxisome proliferator-activated receptor alpha (PPARα) has been shown to reprogram tumor metabolism and exhibits great potential for treating anti-oral tumorigenesis.  Methods: In this study, we used a pathway-based strategy to explore possible functional pathways involved in the anticancer activity of PPARα in oral cancer cells through next-generation sequencing (NGS) and bioinformatic approaches.  Results: We found that 3919 genes were upregulated and 1060 genes were downregulated through PPARα activation. These genes were mainly involved in the proteasomal, mRNA surveillance, spliceosomal, RNA transport, and RNA degradation pathways, as indicated by GO and KEGG enrichment analysis. Importantly, a total of 13 upregulated genes in the RNA degradation pathway were identified including 3 core exosome factor genes ( RRP43, RRP42,  and  CSL4 ), 2 TRAMP complex genes ( TRF4  and  Mtr4 ), 2 exosome cofactor genes ( RRP6  and  MPP6 ), 2 CCR4-NOT complex genes ( CNOT2  and  CNOT3 ), 2 Ski complex genes ( SKI2  and  Ski3 ), 1 decapping complex gene ( EDC4 ), and 1 gene involved in 5’ exoribonuclease activity ( XRN1 ).  Conclusion: Our findings suggest that the activation of PPARα to upregulate the RNA degradation pathway might provide a new strategy for oral cancer treatment.

The RNA degradation pathway is involved in PPARα-modulated anti-oral tumorigenesis