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pubmed-article:8047985pubmed:abstractTextGastrin regulates growth of human colon cancer cells by activation of the cyclic adenosine monophosphate (cAMP)-dependent protein kinase A (PKA). Gastrin and 8-Br-cAMP, a membrane-permeable cAMP analog, inhibit growth of HCT116 cells; both stimulate growth of LoVo cells. This dual effect on growth may be explained by relative amounts of the regulatory subunit (RI alpha or RII beta) of PKA within the cancer cells. Antisense oligodeoxynucleotides (ASO) to either RI alpha or RII beta inhibit protein translation of the target mRNA by sequence-specific binding; subsequently, cellular PKA content and the cAMP-mediated growth may be altered. We determined whether ASO to either the RI alpha or RII beta subunit altered the cAMP-mediated growth of HCT116 and LoVo human colon cancer cells.lld:pubmed
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pubmed-article:8047985pubmed:pagination189-95; discussion 195-6lld:pubmed
pubmed-article:8047985pubmed:dateRevised2010-3-24lld:pubmed
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pubmed-article:8047985pubmed:year1994lld:pubmed
pubmed-article:8047985pubmed:articleTitleExperimental gene therapy of human colon cancer.lld:pubmed
pubmed-article:8047985pubmed:affiliationDepartment of Surgery, University of Texas Medical Branch, Galveston 77555-0533.lld:pubmed
pubmed-article:8047985pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:8047985pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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