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. 2021 Sep 22;22(19):10201. doi: 10.3390/ijms221910201

Figure 6.

Figure 6

MALAT1 overexpression mediated epithelial ovarian cancer (EOC) progression through enhancing inflammation, cell proliferation, and metastasis, while reducing cell apoptosis: A schematic in vitro model for the overexpression of MALAT1 regulating different functional molecules with similar significance levels in both (A–C) HTB75 and (A–C) OVCAR3 cells through upregulation of IL-1β (*** p < 0.001), Cox2 (** p < 0.01 and *** p < 0.001, respectively), PGE2 (***p < 0.001), YAP (** p < 0.01), Vimentin (** p < 0.01), Cyclin D1 (* p < 0.05), Bcl2 (** p < 0.01 and *** p < 0.001, respectively), and zinc finger E-box-binding 2 (ZEB2) (** p < 0.01 and * p < 0.05, respectively), and downregulation of tumor necrosis factor (TNF)-α (* p < 0.05), interleukin (IL)-6 (** p < 0.01), and E-cadherin (** p < 0.01) mRNA levels by a real-time PCR analysis. Moreover, (D) protein levels of phosphorylated (p)-phosphatidylinositol 3-kinase (PI3K) (*** p < 0.001 and * p < 0.05, respectively), p-Akt (** p < 0.01), p-P38 (*** p < 0.001), p-NFκB (*** p < 0.001 and * p < 0.05, respectively), and Bcl2 (* p < 0.05) were also significantly upregulated in MALAT1-overexpressing HTB75 and OVCAR3 cells by a Western blot analysis. (E) Functional mechanisms of MALAT1 overexpression in EOC samples include promotion of inflammation, cell proliferation, and metastasis, combined with inhibition of cellular apoptosis, thereby triggering tumor progression in EOCs. Data shown are the mean ± SD of three independent experiments.