VIP-ellipticine derivatives inhibit the growth of breast cancer cells

Moody, Terry W.; Czerwinski, Grzegorz; Tarasova, N.; Michejda, Christopher J.

doi:10.1016/s0024-3205(02)01741-1

Cited by 32 publications

(36 citation statements)

References 15 publications

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“…Moody et al have coupled ellipticine to VIP by tera-or pentapeptide and investigated the effects of the derivatives on VIPexpressed breast cancer cells. 22 Their results were in agreement with those reported here. The VIP-ellipticine conjugate competed against 125 I-VIP binding to breast cancer cells and inhibited the clonal growth of breast cancer cells.…”

Section: Discussionsupporting

confidence: 92%

“…The result indicate that VIP-ASON can be recognized by VIP receptor on HT29 colon cancer cells, although with somewhat reduced affinity as compared with unmodified VIP. 22 In vivo pharmacokinetics of the VIP-125 I-ASON…”

Section: Vip-ason Bind To Colon Cancer Cells With High Affinitymentioning

confidence: 99%

“…[16][17][18][19][20] It has shown that most primary human tumors, including human colon cancer, express VIP receptors at high incidence and high density, and ligands are internalized by cells possessing VIP receptor subsequent to endocytosis. 21,22 Thereby, the use of VIP as a vector for carrying radiolabeled ASON into a specific location inside a tumor cell contributes an attractive delivery system.…”

mentioning

confidence: 99%

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Antitumor effects of radioiodinated antisense oligonuclide mediated by VIP receptor

Tan

et al. 2004

Cancer Gene Ther

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Section: Discussionsupporting

confidence: 92%

Section: Vip-ason Bind To Colon Cancer Cells With High Affinitymentioning

confidence: 99%

mentioning

confidence: 99%

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Antitumor effects of radioiodinated antisense oligonuclide mediated by VIP receptor

Tan

et al. 2004

Cancer Gene Ther

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“…PACAP-27 addition to lung cancer cells causes increased cAMP, ERK phosphorylation, c-fos mRNA and VEGF expression (Draoui et al 1996;Moody et al 2002a). PACAP stimulates the growth of lung cancer (NCI-H345 cells; Moody et al 1993a), pancreatic carcinoma (AR42-J cells; Buscail et al 1992), and colon cancer cells (Bon cells; Germano et al 2009).…”

Section: Discussionmentioning

confidence: 99%

Pituitary Adenylate Cyclase-Activating Polypeptide Causes Increased Tyrosine Phosphorylation of Focal Adhesion Kinase and Paxillin

2011

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The effects of pituitary adenylate cyclase-activating polypeptide (PACAP) on tyrosine phosphorylation of focal adhesion kinase (FAK) and paxillin were investigated using lung cancer cells. Addition of PACAP-27 or PACAP-38 but not vasoactive intestinal peptide to NCI-H838 or NCI-H1299 human lung cancer cells significantly increased the tyrosine phosphorylation of FAK or paxillin. The increase in FAK or paxillin tyrosine phosphorylation caused by addition of PACAP-27 to NCI-H838 cells was inhibited by PACAP(6-38), a PAC1-receptor (R) antagonist. The increase in FAK or paxillin tyrosine phosphorylation caused by 100 nM PACAP-27 was maximal 2 min after addition to NCI-H838 cells. The effects of PACAP at stimulating FAK and paxillin tyrosine phosphorylation were reversed by cytochalasin D and genistein which inhibit actin polymerization and tyrosine kinase activity, respectively. The effects of PACAP at stimulating FAK and paxillin tyrosine phosphorylation were reversed by U-73122 but not H89 which inhibit phospholipase C and protein kinase A, respectively. The results show that PAC1-R regulates FAK and paxillin tyrosine phosphorylation in lung cancer cells as a result of increased phosphatidylinositol turnover but not adenylyl cylase stimulation.

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“…The overexpression of peptide receptors by the tumor can be used for receptor-targeted delivery of peptide receptor cytotoxic agents [35]. Previously, we reported that VIP-ellipticine (E) conjugates were cytotoxic for lung and breast cancer cells [26]. VIP-LALA-E was internalized by cancer cells containing VPAC 1 -R, and subsequently metabolized by proteolytic enzymes.…”

Section: Introductionmentioning

confidence: 99%

Vasoactive intestinal peptide–camptothecin conjugates inhibit the proliferation of breast cancer cells

et al. 2007

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The effects of vasoactive intestinal peptide camptothecin (VIP-CPT) conjugates were investigated on breast cancer cells and cells transfected with VIP receptors (R). (Ala 2,8,9,19,24.25.27 , Nle 17 , Lys 28 )VIP, (A-NL-K)VIP, was synthesized and Lys 28 was coupled to a linker, N-methyl-aminoethyl-glycine, L2, which formed a carbamate bond with CPT. The resulting (A-NL-K)VIP-L2-CPT was cytotoxic for MCF7 breast cancer cells, which have VPAC 1 -R, with IC 50 values of 380 and 90 nM using the MTT and clonogenic assays, respectively.

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VIP-ellipticine derivatives inhibit the growth of breast cancer cells

Cited by 32 publications

References 15 publications

Antitumor effects of radioiodinated antisense oligonuclide mediated by VIP receptor

Antitumor effects of radioiodinated antisense oligonuclide mediated by VIP receptor

Pituitary Adenylate Cyclase-Activating Polypeptide Causes Increased Tyrosine Phosphorylation of Focal Adhesion Kinase and Paxillin

Vasoactive intestinal peptide–camptothecin conjugates inhibit the proliferation of breast cancer cells

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