Mixtures of persistent organic pollutants increase ovarian granulosa tumor cell line migration and spheroid invasion by upregulating MMP2 expression and activity via IGF1R

Tetrachlorobisphenol A and bisphenol AF induced cell migration by activating PI3K/Akt signaling pathway via G protein‐coupled estrogen receptor 1 in SK‐BR‐3 cells

“…A cell suspension at a density of 5 × 10 5 cells/ml in serum‐free (SF) medium was plated into 6‐well plates. When confluent, cells was pretreated for 3 h with mitomycin C (Sigma‐Aldrich) to inhibit cell proliferation 33 . After that, an artificial scratch was then created using a sterilized 10 μl pipette tip.…”

“…When confluent, cells was pretreated for 3 h with mitomycin C (Sigma-Aldrich) to inhibit cell proliferation. 33 After that, an artificial scratch was then created using a sterilized 10 μl pipette tip. The cells were washed in D-Hanks 3 times to remove floating cells created by the scratch.…”

Environmental Exposure to Persistent Organic Pollutants and Its Association with Endometriosis Risk: Implications in the Epithelial–Mesenchymal Transition Process

“…Other soluble factors, such as the RRM2 gene product, promote EMT by targeting JAK2/STAT3 intracellular cascade [63]. To date, most of the efforts made to address adverse effects associated with human exposure to POPs did not focus on the physiopathological changes underlying hormone-dependent diseases, although in vitro evidence suggests that exposure to some POPs may promote molecular biomarkers related to enhanced migration and invasiveness ability of ovarian granulosa cancer cells such as MMPs [64]. Moreover, Zucchini-Pascal et al [65] pointed out that POPs may orchestrate EMT in human primary cultured hepatocytes, observing the repression of epithelial markers (cell-cell junctions and E-cadherin) and increased the abundance of various mesenchymal genes.…”