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. 2023 Aug 16;13(8):1253. doi: 10.3390/biom13081253

Figure 2.

Figure 2

Crosstalk between IL-6 signaling and the PI3K/AKT/mTOR pathway in EAOC. (1) IL-6 is a physiological target of ARID1A tumor-suppressor activity, which is frequently deficient in EAOC [75]. (2) IL-6 expression is promoted by PI3K, including its catalytic subunit PIK3CA, which is commonly amplified in EAOC [101]. (3) IL-6 triggers the JAK-STAT signaling pathway, which, in turn, has been shown to interact directly with the p58a regulatory subunit of PI3K and to upregulate the expression of AKT [102,103,104]. (4) IL-6 induces the expression of miR-21, a microRNA that impedes PTEN translation and is increased in EAOC [105,106]. ARID1A, AT-rich interaction domain 1A; IL-6, Interleukin 6; PI3K, Phosphatidylinositol-3-kinase; PIK3CA, Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha; JAK, Janus kinase; STAT, signal transducer and activator of transcription protein; AKT, Protein kinase B; miR-21, microRNA-21; PTEN, Phosphatase, and tensin homolog.