English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Zendy Plus

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Zendy Tools

Zendy Open

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 ( VPAC 1 and  VPAC 2) 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.

Vasoactive intestinal peptide increases apoptosis of hepatocellular carcinoma by inhibiting the cAMP /Bcl‐ xL pathway