Inhibition of CACO-2 cell proliferation by (n-3) fatty acids: possible mediation by increased secretion of insulin-like growth factor binding protein-6

Kim, Eun J.; Kim, Wha Y.; Kang, Young Jong; Ha, Yeong Lae; Bach, Leon A.; Park, Jung H.Y.

doi:10.1016/s0271-5317(00)80022-6

Cited by 23 publications

(26 citation statements)

References 31 publications

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“…IGFBP-6 may be antitumorigenic for colon cancer as evidenced by lower levels in a metastatic than a non-metastatic cell line (Futschik, et al 2002), and in a multidrug-resistant than in a sensitive colon cancer cell line (Fan, et al 2004). Exogenous IGFBP-6 inhibited IGF-II-induced proliferation and adhesion of colon cancer cells (Leng, et al 2001), and IGFBP-6 expression was increased in colon cancer cells by (n-3) fatty acids and retinoic acid, both of which inhibit proliferation (Kim, et al 2000(Kim, et al , 2001. Coculture of colon cancer cells with normal colonic epithelial cells decreased IGFBP-6 secretion, and IGFBP-6 expression was dramatically decreased in normal colonic epithelial cells undergoing epithelial-mesenchymal transdifferentiation, a process that is implicated in tumorigenesis (Zeng, et al 2013).…”

Section: Colon Cancermentioning

confidence: 99%

Recent insights into the actions of IGFBP-6

Bach

2015

J. Cell Commun. Signal.

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IGFBP-6 is an O-linked glycoprotein that preferentially binds IGF-II over IGF-I. It is a relatively selective inhibitor of IGF-II actions including proliferation, survival and differentiation of a wide range of cells. IGFBP-6 has recently been shown to have a number of IGF-independent actions, including promotion of apoptosis in some cells and inhibition of angiogenesis. IGFBP-6 also induces migration of tumour cells including rhabdomyosarcomas by an IGF-independent mechanism. This chemotactic effect is mediated by MAP kinases. IGFBP-6 binds to prohibitin-2 on the cell surface and the latter is required for IGFBP-6-induced migration by a mechanism that is independent of MAP kinases. IGFBP-6 may enter the nucleus and modulate cell survival and differentiation. IGFBP-6 expression is decreased in a number of cancer cells and it has been postulated to act as a tumour suppressor. IGFBP-6 expression is increased in a smaller number of cancers, which may reflect a compensatory mechanism to control IGF-II actions or IGF-independent actions. The relative balance of IGF-dependent and IGF-independent actions of IGFBP-6 in vivo together with the related question regarding the roles of IGFBP-6 binding to IGF and non-IGF ligands are keys to understanding the physiological role of this protein.

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Section: Colon Cancermentioning

confidence: 99%

Recent insights into the actions of IGFBP-6

Bach

2015

J. Cell Commun. Signal.

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“…Though little data on the in vitro effect of PUFAs on IGF-1 are available, IGF-1 may be involved in the observed effects of PUFAs on osteoclastogenesis. PUFAs such as AA, EPA and DHA inhibit both osteoblast and Caco-2 adenocarcinoma cell proliferation [26,85]. EPA and DHA both reduced IGF-II and increased IGFBP-6 in Caco-2 cells resulting in less free IGF-II thereby inhibiting cell proliferation [85].…”

Section: Effects Of Dietary Polyunsaturated Fatty Acids and Their Promentioning

confidence: 99%

“…PUFAs such as AA, EPA and DHA inhibit both osteoblast and Caco-2 adenocarcinoma cell proliferation [26,85]. EPA and DHA both reduced IGF-II and increased IGFBP-6 in Caco-2 cells resulting in less free IGF-II thereby inhibiting cell proliferation [85]. It can thus be speculated that the latter may also be the mechanism involved whereby EPA and DHA suppress osteoblast proliferation.…”

Section: Effects Of Dietary Polyunsaturated Fatty Acids and Their Promentioning

confidence: 99%

Long-chain polyunsaturated fatty acids: Selected mechanisms of action on bone

Kruger

Coetzee

Haag

et al. 2010

Progress in Lipid Research

142

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“…After serum starvation, fresh serum-free medium with or without the indicated concentrations of CLA was replaced. Fatty acids were complexed to essentially fatty acid-free BSA, with the molar ratio of fatty acid to BSA being 4:1 (Kim et al, 2000). Medium was changed every 2 days.…”

Section: Cell Culturementioning

confidence: 99%

Inhibition of colon cancer cell proliferation by the dietary compound conjugated linoleic acid is mediated by the CDK inhibitor p21^CIP1/WAF1

Lim

Tyner

Park

et al. 2005

Journal Cellular Physiology

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Our previous studies indicated that dietary conjugated linoleic acid (CLA) inhibits colon tumor cell proliferation in vitro and in vivo. To identify mechanisms by which CLA regulates growth arrest, the HT-29 human colon carcinoma cell line was treated with various physiological concentrations of CLA and analyzed by flow cytometry. We detected a dose-dependent increase in the percentage of cells arrested in G1 after CLA treatment that was accompanied by induction of the cyclin dependent kinase (CDK) inhibitor p21CIP1/WAF. CLA addition also led to increased p21 expression in HCT116 and SW480 cells, indicating that p21 induction is a general consequence of CLA treatment in colon cancer cells. Since both HT-29 and SW480 cells have mutant p53, our data indicate that p53 is not essential for induction of p21. In addition to an increase in p21 levels, HT-29 cell growth arrest was also accompanied by moderate decreases in Cyclin A, D1, E, and proliferating cell nuclear antigen (PCNA) levels. Following CLA treatment, p21 associated with and inhibited CDK4 and CDK2, and this correlated with reduced phosphorylation of retinoblastoma proteins. Increased association of p21 with PCNA was also detected. Dietary CLA inhibits cell cycle progression by inducing p21, which negatively regulates the growth promoting activities of CDK/cyclins and PCNA. These studies indicate that physiological concentrations of CLA inhibit growth of colon cancer cells with either wild-type or mutant p53, and may have therapeutic benefits in vivo.

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Inhibition of CACO-2 cell proliferation by (n-3) fatty acids: possible mediation by increased secretion of insulin-like growth factor binding protein-6

Cited by 23 publications

References 31 publications

Recent insights into the actions of IGFBP-6

Recent insights into the actions of IGFBP-6

Long-chain polyunsaturated fatty acids: Selected mechanisms of action on bone

Inhibition of colon cancer cell proliferation by the dietary compound conjugated linoleic acid is mediated by the CDK inhibitor p21^CIP1/WAF1

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Inhibition of CACO-2 cell proliferation by (n-3) fatty acids: possible mediation by increased secretion of insulin-like growth factor binding protein-6

Cited by 23 publications

References 31 publications

Recent insights into the actions of IGFBP-6

Recent insights into the actions of IGFBP-6

Long-chain polyunsaturated fatty acids: Selected mechanisms of action on bone

Inhibition of colon cancer cell proliferation by the dietary compound conjugated linoleic acid is mediated by the CDK inhibitor p21CIP1/WAF1

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Inhibition of colon cancer cell proliferation by the dietary compound conjugated linoleic acid is mediated by the CDK inhibitor p21^CIP1/WAF1