Related Experiment Video
Updated: Aug 14, 2026

An Orthotopic Murine Model of Human Prostate Cancer Metastasis
Published on: September 18, 2013
The contribution of inhibins and activins to malignant prostate disease
G P Risbridger1, S L Mellor, S J McPherson
1Monash Institute of Reproduction and Development, Monash University, Monash Medical Centre, Clayton, 3168, Victoria, Australia. gail.risbridger@med.monash.edu.au
Abstract:
The normal human prostate expresses inhibin and activin subunits. In prostate cancer, the inhibin alpha subunit gene is down regulated and this is associated with loss of heterozygosity (LOH) at the gene locus and methylation of the promoter. These data support the hypothesis that the inhibin alpha subunit is tumor suppressive in the prostate. The pluripotent effects of activins and the similarities to transforming growth factor beta (TFGbeta) suggest a role for activins in progression to malignancy, whereby, the normal growth inhibitory action of activin A observed on benign cells is lost with the acquisition of activin resistance in prostate cancer cells. The mechanisms of rendering tumor cells resistant to activin A may include: alteration in activin binding protein (follistatin) synthesis and/or dimerisation with activin beta(C) to form novel activin dimers. The contribution of the activin signalling cascade to malignancy requires further evaluation to identify the synergies and differences to other members of the TGFbeta superfamily.
Related Concept Videos
Abnormal Proliferation
The Tumor Microenvironment
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
Cancer Cell Migration through Invadopodia
The Intrinsic Apoptotic Pathway
Activation of Integrins
In "outside-in signaling," external factors in the extracellular space bind to exposed ligand binding sites on integrins. This causes the inactive protein to undergo a conformational change to become active. Integrins are often clustered on the cell membrane. Repetitive and regularly spaced ligand binding events provide an effective stimulus.

