69. The Induction of Epithelial-Mesenchymal Transition by PTEN in Colorectal Cancer

Bowen, Kanika A.; Zhou, Binhua P.; Doan, Hung Q.; Rychahou, Piotr G.; Evers, B. Mark

doi:10.1016/j.jss.2008.11.082

Cited by 36 publications

(44 citation statements)

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“…Furthermore, it was found that the mutation in the ATP motif of PTEN may affect its subcelluar localization and tumor suppressive function (11,26). In our study, PTEN protein was mostly expressed in the cytoplasm, but not in the nucleus, and no significant difference was observed between CRC, adenoma and normal colorectal mucosa, which was consistent with previous studies (27,28). However, whether the unmatched paired design and different genetic backgrounds were responsible for the results requires additional studies.…”

Section: Discussionsupporting

confidence: 91%

Expression of PPARγ and PTEN in human colorectal cancer: An immunohistochemical study using tissue microarray methodology

et al. 2011

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Abstract. Although aberrations of peroxisome proliferatoractivated receptor γ (PPARγ) and phosphatase and tensin homolog (PTEN) expression have been identified in several other cancer types, certain previous studies have revealed that PPARγ is abundant in normal and malignant tissue in the colon. The question of whether aberrant PTEN is involved in the initial stage or is a later event during colorectal carcinogenesis remains controversial. Relatively few studies have focused on the correlation of expression of PPARγ and PTEN in various tissues. In the present study, paraffin-embedded blocks from 139 patients with CRC, 18 adenomatous polyps and 50 paired paracancerous benign mucosas were selected and analysed in 4 tissue microarray (TMA) blocks comprising 104, 72, 130 and 54 cores, respectively. Expression of PPARγ and PTEN was examined using immunohistochemical staining on TMAs. There were no significant differences in the expression of PPARγ (P=0.055) and PTEN (P=0.100) between the colorectal cancers, adenomas and paracancerous mucosas. However, correlations of PPARγ expression with clinical stage (P=0.004) and PTEN expression with histological grade (P=0.006) and distant metastasis (P=0.015) were demonstrated in the CRC specimens. Although the differences in PPARγ and PTEN protein expression in human colorectal cancer may not be considered as early diagnostic markers, our results indicate that CRCs with a low expression or deletion of PTEN may progress towards invasion and even metastasis; thus, PTEN may have potential as a prognostic marker in human CRC.

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Section: Discussionsupporting

confidence: 91%

Expression of PPARγ and PTEN in human colorectal cancer: An immunohistochemical study using tissue microarray methodology

et al. 2011

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“…However, to the best of our knowledge, the role of PTEN in OSCC has been rarely reported. Although the mechanism remains to be elucidated, an abnormal decrease of PTEN has been demonstrated in the majority of types of tumor (6,(25)(26)(27)(28)(29)(30)(31). In the present study, a significant reduction in PTEN expression was observed in the tumor tissues, blood and saliva of patients with gingival carcinoma compared with control patients.…”

Section: Discussionsupporting

confidence: 48%

“…The downregulation or deletion of PTEN has a role in apoptosis, cell cycle and cell migration, and is associated with the development of various human malignancies (44). Previous research on the effect of PTEN on tumorigenesis has predominantly focused on endometrial cancer, glioma, prostate cancer, breast cancer and melanoma (25)(26)(27)(28)(29)(30)(31). However, to the best of our knowledge, the role of PTEN in OSCC has been rarely reported.…”

Section: Discussionmentioning

confidence: 99%

Elucidating the mechanism of miRNA-214 in the regulation of gingival carcinoma

Gong

Yang

Tian

2017

Experimental and Therapeutic Medicine

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Abstract. The aim of the present study was to evaluate the expression levels of microRNA (miRNA)-214 in tumor tissue, blood and saliva of patients with gingival carcinoma, and to investigate the mechanisms underlying the infiltration and invasion of gingival carcinoma. Between January 2013 and March 2015, blood and saliva samples, gingival carcinoma tumor specimens and peritumoral tumor tissues were harvested from 56 patients with gingival carcinoma. Blood and saliva samples were also harvested from 33 control patients without gingival carcinoma. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was performed to detect miRNA-214 and protein tyrosine phosphatase gene (PTEN) mRNA levels. Western blotting and ELISA were performed to detect PTEN protein levels. The results of RT-qPCR demonstrated that the expression of PTEN mRNA in tumor tissues, blood and saliva of patients with gingival carcinoma were significantly decreased compared with that of the control group (P<0.05). These findings were consistent were consistent with the results of PTEN protein expression detected via western blotting and ELISA in these samples (P<0.05). Conversely, the expression levels of miRNA-214 in these samples were significantly increased (P<0.05) in patients with gingival carcinoma compared with the control group. The decreased expression of PTEN may be associated with the expression of miRNA-214. miRNA-214 may regulate infiltration and invasion of gingival carcinoma via PTEN. These results suggest that miRNA-214 may be used as a marker of gingival carcinoma.

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“…Binding of PTEN to the PDZ domain of MAGI2 enhanced PTEN protein stability and the activity of the downregulating PI3K/Akt signaling cascade (41,42). Previous studies demonstrated that degradation or loss of PTEN caused PI3K/Akt activation, elicited cell migration and proliferation, and induced the EMT phenomenon (27,(43)(44)(45). Absence of PTEN-MAGI2 binding induced PTEN phosphorylation and affected PTEN stability (41,46).…”

Section: Discussionmentioning

confidence: 99%

MiR-134/487b/655 Cluster Regulates TGF-β–Induced Epithelial–Mesenchymal Transition and Drug Resistance to Gefitinib by Targeting MAGI2 in Lung Adenocarcinoma Cells

Kitamura

Seike

Okano

et al. 2014

Molecular Cancer Therapeutics

168

135

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Epithelial-mesenchymal transition (EMT) has recently been recognized as a key element of cell invasion, migration, metastasis, and drug resistance in several types of cancer, including non-small cell lung cancer (NSCLC). Our aim was to clarify microRNA (miRNA)-related mechanisms underlying EMT followed by acquired resistance to epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) in NSCLC. miRNA expression profiles were examined before and after transforming growth factor b1 (TGF-b1) exposure in four human adenocarcinoma cell lines with or without EMT. Correlation between expressions of EMT-related miRNAs and resistance to EGFR-TKI gefitinib was evaluated. miRNA array and real-time quantitative reverse transcription PCR (qRT-PCR) revealed that TGF-b1 significantly induced overexpression of miR-134, miR-487b, and miR-655, which belong to the same cluster located on chromosome 14q32, in lung adenocarcinoma cells with EMT. MAGI2 (membrane-associated guanylate kinase, WW, and PDZ domain-containing protein 2), a predicted target of these miRNAs and a scaffold protein required for PTEN, was diminished in A549 cells with EMT after the TGF-b1 stimulation. Overexpression of miR-134 and miR-487b promoted the EMT phenomenon and affected the drug resistance to gefitinib, whereas knockdown of these miRNAs inhibited the EMT process and reversed TGF-b1-induced resistance to gefitinib. Our study demonstrated that the miR-134/487b/655 cluster contributed to the TGF-b1-induced EMT phenomenon and affected the resistance to gefitinib by directly targeting MAGI2, in which suppression subsequently caused loss of PTEN stability in lung cancer cells. The miR-134/miR-487b/miR-655 cluster may be a new therapeutic target in patients with advanced lung adenocarcinoma, depending on the EMT phenomenon. Mol Cancer Ther; 13(2); 444-53. Ó2013 AACR.

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69. The Induction of Epithelial-Mesenchymal Transition by PTEN in Colorectal Cancer

Cited by 36 publications

References 0 publications

Expression of PPARγ and PTEN in human colorectal cancer: An immunohistochemical study using tissue microarray methodology

Expression of PPARγ and PTEN in human colorectal cancer: An immunohistochemical study using tissue microarray methodology

Elucidating the mechanism of miRNA-214 in the regulation of gingival carcinoma

MiR-134/487b/655 Cluster Regulates TGF-β–Induced Epithelial–Mesenchymal Transition and Drug Resistance to Gefitinib by Targeting MAGI2 in Lung Adenocarcinoma Cells

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