CAI inhibits the growth of small cell lung cancer cells

Moody, Terry W.; Chiles, Jessica; Moody, Elizabeth; Sieczkiewicz, Gregory J.; Kohn, Elise C.

doi:10.1016/s0169-5002(02)00525-1

Cited by 33 publications

(26 citation statements)

References 34 publications

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“…Thus, we hypothesized that if PAMP is an angiogenic factor that may be acting through GRP receptors, GRP itself may have an impact on angiogenesis. There are a few reports in the literature that further support this hypothesis, for example binding of GRP to rat brain microvascular endothelial cells has been reported (Vigne et al, 1995), and exposure of prostate and lung cancer cells to GRP has been shown to stimulate secretion of proangiogenic factors (Levine et al, 2003;Moody et al, 2003a).…”

Section: Introductionmentioning

confidence: 98%

Gastrin-releasing peptide (GRP) induces angiogenesis and the specific GRP blocker 77427 inhibits tumor growth in vitro and in vivo

et al. 2005

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Angiogenesis is becoming a major target for antitumor therapies, and identifying new angiogenic factors and their specific inhibitors may provide new avenues for tumor management. Here we identify gastrin-releasing peptide (GRP) as a new angiogenic molecule that is secreted by tumors and acts directly upon GRP receptors in the endothelial cells. Addition of GRP increases endothelial cell migration and cord formation in vitro, and induces angiogenesis in an in vivo assay. We have recently identified a small molecule GRP blocker, compound 77427. This inhibitor significantly reduced endothelial cell cord formation in vitro and angiogenesis in vivo. Conversely, when applied to VEGF-induced angiogenesis, the small molecule did not have any effect, demonstrating its specificity. Furthermore, this GRP blocker was able to reduce lung tumor cell growth in vitro as demonstrated by MTT and clonogenic assays. When applied to a xenograft model with lung cancer cells, compound 77427 reduced tumor volume to undetectable sizes, although when the treatment was suspended, tumors began to grow again at normal rates. Our collective observations indicate that GRP is a new angiogenic peptide and that its inhibition offers an attractive tool to reduce tumor burden.

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Section: Introductionmentioning

confidence: 98%

Gastrin-releasing peptide (GRP) induces angiogenesis and the specific GRP blocker 77427 inhibits tumor growth in vitro and in vivo

et al. 2005

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“…The CCK2R regulates the growth of normal and neoplastic gastrointestinal mucosal cells and the growth of different cells outside the digestive system (3)(4)(5)(6)(7)(8)(9)(10)(11). The growth-promoting action of the CCK2R has led to extensive investigations of its role in carcinogenesis and its expression in cancer.…”

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confidence: 99%

Signaling through cholesterol esterification: a new pathway for the cholecystokinin 2 receptor involved in cell growth and invasion

Paillasse

Médina

Amouroux

et al. 2009

Journal of Lipid Research

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“…It mediates the normal physiological function of gastrin. Gastrin has proliferative effects on various malignancies including gastric, colorectal, pancreatic, medullary thyroid cancers, small cell lung cancer as well as tumors of the central and peripheral nervous systems through CCK-B receptors [11][12][13][14][15][16][17] . Coexpression of gastrin gene and CCK-B receptor in cancer tissues in vivo or cell lines in vitro may suggest the existence of autocrine or paracrine pathways, through which gastrin exerts its physiological or pathological effects.…”

Section: Discussionmentioning

confidence: 99%

Coexpression of cholecystokinin-B/gastrin receptor and gastrin gene in human gastric tissues and gastric cancer cell line

Zhou¹,

Chen²,

Zhang³

et al. 2004

WJG

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AIM:To compare the expression patterns of cholecystokinin-B (CCK-B)/gastrin receptor genes in matched human gastric carcinoma and adjacent non-neoplastic mucosa of patients with gastric cancer, inflammatory gastric mucosa from patients with gastritis, normal stomachs from 2 autopsied patients and a gastric carcinoma cell line (SGC-7901), and to explore their relationship with progression to malignancy of human gastric carcinomas. METHODS:RT-PCR and sequencing were employed to detect the mRNA expression levels of CCK-B receptor and gastrin gene in specimens from 30 patients with gastric carcinoma and healthy bordering non-cancerous mucosa, 10 gastritis patients and normal stomachs from 2 autopsied patients as well as SGC-7901. The results were semi-quantified by normalizing it to the mRNA level of β-actin gene using Lab Image software. The sequences were analyzed by BLAST program. RESULTS:CCK-B receptor transcripts were detected in all of human gastric tissues in this study, including normal, inflammatory and malignant tissues and SGC-7901. However, the expression levels of CCK-B receptor in normal gastric tissues were higher than those in other groups (P<0.05), and its expressions did not correlate with the differentiation and metastasis of gastric cancer (P>0.05). On the other hand, gastrin mRNA was detected in SGC-7901 and in specimens obtained from gastric cancer patients (22/30) but not in other gastric tissues, and its expression was highly correlated with the metastases of gastric cancer (P<0.05).

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CAI inhibits the growth of small cell lung cancer cells

Cited by 33 publications

References 34 publications

Gastrin-releasing peptide (GRP) induces angiogenesis and the specific GRP blocker 77427 inhibits tumor growth in vitro and in vivo

Gastrin-releasing peptide (GRP) induces angiogenesis and the specific GRP blocker 77427 inhibits tumor growth in vitro and in vivo

Signaling through cholesterol esterification: a new pathway for the cholecystokinin 2 receptor involved in cell growth and invasion

Coexpression of cholecystokinin-B/gastrin receptor and gastrin gene in human gastric tissues and gastric cancer cell line

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