| Abstract | This research aimed to explore the phenotypic changes apparent in cancer cells upon inhibiting MAPK14 minor intron splicing. MAPK14 is a member of the Mitogen Activated Protein kinase family which integrates various biochemical signals involved in a variety of cellular processes including development, differentiation, proliferation, regulation and transcription [1]. MAPK14 is activated like other members of the kinase family by environmental stress and proinflammatory cytokines [1]. MAPK14 substrate including the cell cycle regulator CDC25B and the tumour suppressor P53 suggest that it functions in stress related transcription and cell cycle regulation [1]. The main question explored was the effects of inhibiting this gene at the splicing level on the progression and proliferation of cancer cells either by itself or by also affecting other genes. To do so, I utilized bioinformatics and molecular techniques to knock down the gene coding this MAPK14 in MDA-MB-23 breast cancer cells. The result showed that MAPK14 inhibition lowers cell proliferation and migration. With RNA extraction MAPK14 inhibition seems to increase RNA production demonstrating its suppressor function. Yet with protein production, it seems like less is produced when MAPK14 is inhibited. This will set the foundation for future therapeutic and diagnostic approaches to cancer by setting this kinase as a target.
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