Impact of PTEN on the expression of insulin-like growth factors (IGFs) and IGF-binding proteins in human gastric adenocarcinoma cells

Yi, Ho-Keun; Kim, Sun‐Young; Hwang, Pyoung-Han; Kim, Chan Young; Yang, Doo-Hyun; Oh, Youngman; Lee, Dae-Yeol

doi:10.1016/j.bbrc.2005.03.045

Cited by 40 publications

(22 citation statements)

References 22 publications

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“…Tumor suppressor genes, including p53 (79) and phosphatase and tensin homolog (80), have also been shown to up-regulate IGFBP-3 at the transcriptional level.…”

Section: Igfbp-3 and Igfbp-3r Igfbp-3mentioning

confidence: 99%

Targeting Insulin-Like Growth Factor-I and Insulin-Like Growth Factor–Binding Protein-3 Signaling Pathways. A Novel Therapeutic Approach for Asthma

Lee

Kim

et al. 2014

Am J Respir Cell Mol Biol

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“…Tumor suppressor genes, including p53 (79) and phosphatase and tensin homolog (80), have also been shown to up-regulate IGFBP-3 at the transcriptional level.…”

Section: Igfbp-3 and Igfbp-3r Igfbp-3mentioning

confidence: 99%

Targeting Insulin-Like Growth Factor-I and Insulin-Like Growth Factor–Binding Protein-3 Signaling Pathways. A Novel Therapeutic Approach for Asthma

Lee

Kim

et al. 2014

Am J Respir Cell Mol Biol

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“…Mutation or loss of function of PTEN is frequent in a wide range of cancers including glioblastoma multiforme (9), gastric cancer (10), endometrial cancer (11,12), ovarian cancer (12) and lung cancer (13). PTEN can decrease the synthesis of IGF-I, -II and IGF-1R, which in turn generates an autocrine loop to downregulate Akt activation (14,15). Therefore, high Akt phosphorylation is frequently associated with loss of PTEN, leading to chemorestistance and poor prognosis in cancer patients (16,17).…”

Section: Introductionmentioning

confidence: 99%

The phosphatidylinositol 3-kinase/Akt and c-Jun N-terminal kinase signaling in cancer: Alliance or contradiction? (Review)

Zhao

Wang

2015

International Journal of Oncology

106

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Abstract. The phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway and c-Jun N-terminal kinase (JNK) pathway are responsible for regulating a variety of cellular processes including cell growth, migration, invasion and apoptosis. These two pathways are essential to the development and progression of tumors. The dual roles of JNK signaling in apoptosis and tumor development determine the different interactions between the PI3K/Akt and JNK pathways. Activation of PI3K/ Akt signaling can inhibit stress-and cytokine-induced JNK activation through Akt antagonizing and the formation of the JIP1-JNK module, as well as the activities of upstream kinases ASK1, MKK4/7 and MLK. On the other hand, hyperactivation of Akt and JNK is also found in cancers that harbor EGFR overexpression or loss of PTEN. Understanding the activation mechanism of PI3K/Akt and JNK pathways, as well as the interplays between these two pathways in cancer may contribute to the identification of novel therapeutic targets. In the present report, we summarized the current understanding of the PI3K/Akt and JNK signaling networks, as well as their biological roles in cancers. In addition, the interactions and regulatory network between PI3K/Akt and JNK pathways in cancer were discussed.

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“…We used the AdEasy system (Quantum Biotechnologies, Quebec, Canada) to generate adenovirus as described previously [19]. As a control, Ad/LacZ, which contains an empty vector, was produced.…”

Section: Tissue Samplesmentioning

confidence: 99%

“…Western blots were performed as previously described [19]. In brief, conditioned media or cell lysates were sizefractionated by 12 % SDS-PAGE under non-reducing conditions and electroblotted onto nitrocellulose filters (Hybond; Amersham Pharmacia Biotech, Piscataway, NJ, USA).…”

Section: Western Blot Analysismentioning

confidence: 99%

Insulin-like growth factor binding protein-3 enhances etoposide-induced cell growth inhibition by suppressing the NF-κB activity in gastric cancer cells

Kim

Lee

2015

Mol Cell Biochem

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Nuclear factor-kappaB (NF-κB) is a transcription factor that is activated in various neoplasms, including gastric cancer. Insulin-like growth factor binding protein-3 (IGFBP-3) is a potent tumor suppressor and is significantly suppressed in a variety of cancers. Although IGFBP-3 has been reported to have antiproliferative and proapoptotic effects, the precise mechanisms underlying the action of IGFBP-3 have not been elucidated. In this study, we found an inverse correlation between NF-κB activity and IGFBP-3 expression in patients with gastric cancer. Overexpression of IGFBP-3 resulted in significant inhibition of total and phosphorylated p65 NF-κB and IκB proteins in gastric cancer cells. IGFBP-3 further inhibited the expression of NF-κB-regulated cell adhesion molecules, ICAM-1 and VCAM-1. Finally, the growth inhibition induced by etoposide was significantly enhanced by IGFBP-3 overexpression along with concomitant suppression of NF-κB activity. These findings indicate that IGFBP-3 enhances etoposide-induced cell growth inhibition by blocking the NF-κB signaling pathway in gastric cancer cells. Furthermore, our data suggest that IGFBP-3 could be used as an adjuvant in the treatment of gastric cancer.

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Impact of PTEN on the expression of insulin-like growth factors (IGFs) and IGF-binding proteins in human gastric adenocarcinoma cells

Cited by 40 publications

References 22 publications

Targeting Insulin-Like Growth Factor-I and Insulin-Like Growth Factor–Binding Protein-3 Signaling Pathways. A Novel Therapeutic Approach for Asthma

Targeting Insulin-Like Growth Factor-I and Insulin-Like Growth Factor–Binding Protein-3 Signaling Pathways. A Novel Therapeutic Approach for Asthma

The phosphatidylinositol 3-kinase/Akt and c-Jun N-terminal kinase signaling in cancer: Alliance or contradiction? (Review)

Insulin-like growth factor binding protein-3 enhances etoposide-induced cell growth inhibition by suppressing the NF-κB activity in gastric cancer cells

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