Human ovarian cancer cell morphology, motility, and proliferation are differentially influenced by autocrine TGFβ superfamily signalling

TGFβ superfamily signalling participates in normal and pathophysiologic cellular processes. Despite several reports demonstrating active TGFβ superfamily signalling pathways in OvCa cell lines and primary cultures, few studies examine their functional outcome. Herein we show that primary human ovarian cancer cells possess intact autocrine BMP, TGFβ and activin signalling. Blocking autocrine signalling resulted in differential cellular responses affecting cellular morphology, motility and proliferation. Additionally, BMP4-induced alterations in morphology and motility are dependent on Smad signalling. These results suggest that a balance between BMP and TGFβ/activin signalling may be altered to favour BMP signalling during ovarian cancer metastatic progression.

► Human ovarian cancer cells possess autocrine BMP4, BMP6, TGFβ, and activin signalling.
► Autocrine signalling regulates morphology, cell density, proliferation, and motility.
► BMP4-induced changes are Smad-dependent.
► Mean BMP4 levels in human ascites is 18 pg/mL.
► Balance between BMP and TGFβ signalling may regulate epithelial–mesenchymal status.