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PACAP (6–38) is a PACAP receptor antagonist for breast cancer cells (1999)

Leyton, Julius ; Gozes, Yehoshua ; Pisegna, Joseph ; [et al.]

Springer

Breast cancer research and treatment 56 (1999), S. 175-184

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ISSN: 1573-7217

Keywords: PACAP ; VIP ; breast cancer ; proliferation

Source: Springer Online Journal Archives 1860-2000

Topics: Medicine

Notes: Abstract The effects of pituitary adenylate cyclase activating polypeptide (PACAP) analogs were investigated using breast cancer cells. 125I–PACAP–27 bound with high affinity (Kd=5 nM) to T47D cells (Bmax = 29,000 per cell). Specific 125I–PACAP–27 binding was inhibited half maximally by PACAP–27, PACAP–38, PACAP(6–38) and PACAP(28–38) with IC50 values of 8, 17, 750 and 〉3000 nM, respectively. By RT–PCR, PACAP receptor mRNA was present in MCF–7 and T47D cell lines. Polyclonal antibodies to a PACAP receptor fragment (A–8–C) were elicited. The antibodies were affinity purified, recognized a 60–kDa protein by western blot, and stained malignant cells in breast cancer biopsy specimens by immunohistochemistry. PACAP–27 elevated the cAMP in T47D cells and the increase in cAMP caused by PACAP was inhibited by PACAP(6–38). PACAP–27 stimulated c–fos mRNA in T47D cells and the increase in c-fos gene expression caused by PACAP was reversed by PACAP (6–38). PACAP (6–38) inhibited colony formation using a soft agar assay and inhibited breast cancer xenograft growth in nude mice. These data suggest that PACAP (6–38) functions as a breast cancer PACAP receptor antagonist.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1023/A:1006262611290

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Monoclonal antibody αIR-3 inhibits non-small cell lung cancer growth in vitro and in vivo (1996)

Zia, Farah ; Jacobs, Steve ; Kull, Frederick ; [et al.]

New York, N.Y. : Wiley-Blackwell

Journal of Cellular Biochemistry 63 (1996), S. 269-275

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ISSN: 0730-2312

Keywords: IGF-I ; non-small cell lung cancer ; monoclonal antibodies ; growth ; receptors ; Life Sciences ; Molecular Cell Biology

Source: Wiley InterScience Backfile Collection 1832-2000

Topics: Biology , Chemistry and Pharmacology , Medicine

Notes: The ability of monoclonal antibody (mAb) αI̊-3 to interact with non-small cell lung cancer (NSCLC) cells was investigated. MAb αI̊-3 inhibited specific binding of 125I-IGF-I and 125I-αI̊-3 to a panel of 8 NSCLC cell lines with high affinity (IC50 = 200 and 50 ng/ml, respectively). 125I-αI̊-3 bound with high affinity (Kd = 40 ng/ml) to a single class of sites (Bmax = 8,000/cell) using NCI-H838 cells. 125I-αI̊-3 was internalized when exposed to NCI-H838 or H1299 cells at 37°C but not 4°C. αI̊-3 immunoprecipitated major 90 and 130 kD proteins. IGF-I stimulated and αI̊-3 inhibited the clonal growth of NCI-H1299 cells. αI̊-3 slowed the growth of NCI-H157 and H838 xenografts in nude mice. In a biodistribution study 125I-αI̊-3 was preferentially localized to the tumor as opposed to other organs. These data suggest that IGF-I may be a regulatory agent in NSCLC. © 1996 Wiley-Liss, Inc.This article is a US Government work and, as such, is in the public domain in the United States of America.

Additional Material: 6 Ill.