Study summary · research use only
Vasoactive intestinal peptide increases apoptosis of hepatocellular carcinoma by inhibiting the cAMP/Bcl-xL pathway
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This laboratory study examined vasoactive intestinal peptide (VIP) and its receptors (VPAC1 and VPAC2) in surgically resected hepatocellular carcinoma (HCC) tissue samples and in the HCC cell line Huh7 (species not specified in the abstract). VIP treatment (10-10 M) significantly suppressed proliferation of Huh7 cells, and the authors examined the mechanism of apoptosis, reporting increased caspase-3 and decreased Bcl-xL and cyclic AMP (cAMP) response element-binding protein (CREB), along with reduced CREB phosphorylation. These effects were reversed by a VIP receptor antagonist or the cAMP antagonist Rp-cAMPS, and pretreatment with a cAMP analogue blocked the increased apoptosis, suggesting VIP induces apoptosis via a PKA-independent signaling mechanism. The authors report that their data indicate VIP is associated with apoptosis in HCC through the cAMP/Bcl-xL pathway.
Abstract
Vasoactive intestinal peptide (VIP) is a modulator of inflammatory responses. VIP receptors are expressed in several tumor types, such as colorectal carcinoma. The study described herein was conducted to confirm the presence of VIP and its receptors (VPAC1 and VPAC2) in surgically resected hepatocellular carcinoma (HCC) tissues and in the HCC cell line Huh7. The mechanism responsible for apoptosis of HCC cells was then examined because VIP treatment (10-10 M) significantly suppressed proliferation of Huh7 cells. In examining apoptosis-related proteins, we found caspase-3 to be significantly increased and Bcl-xL and cyclic AMP (cAMP) response element-binding protein (CREB) to be significantly decreased in Huh7 cells cultured with VIP. Furthermore, the CREB level and phosphorylation were reduced. These effects were reversed by the addition of VIP receptor antagonist or cAMP antagonist Rp-cAMPS. Pretreatment with cAMP analogue blocked the increased apoptosis, suggesting that VIP induces apoptosis via a PKA-independent signaling mechanism. Our data indicate that VIP prevents the progression of HCC by apoptosis through the cAMP/Bcl-xL pathway.
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