Mutational Analysis of the PTEN Gene and Its Effects in Esophageal Squamous Cell Carcinoma

Hou, Guoqing; Lu, Zhaoming; Liu, Mingyue; Liu, Hong‐Min; Xue, Liyan

doi:10.1007/s10620-010-1474-0

Cited by 11 publications

(12 citation statements)

References 30 publications

(37 reference statements)

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“…PTEN can act as a tumor suppressor gene, and some studies have shown that deletion of chromosome 10q results in PTEN gene mutations in some tumors, thereby eliminating gene expression (Ohgaki and Kleihues, 2007;Suvasini et al, 2011). One study determined that PTEN gene expression was decreased in esophageal cancer tissues, and that the level of PTEN protein expression was negatively correlated with tumor size, lymph node metastasis, and the staging of esophageal cancer (Hou et al, 2011). The study found that the carcinogenicity of mir-21 was independent of low PTEN gene expression.…”

Section: Discussionmentioning

confidence: 99%

Characterization and effects of miR-21 expression in esophageal cancer

et al. 2015

Genet. Mol. Res.

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ABSTRACT. The aim of this study was to investigate the expression of miR-21 in esophageal cancer and the impact of miR-21 on apoptosis, invasion, and the expression of target genes in esophageal cancer cells. Fluorescence quantitative polymerase chain reaction analysis was used to detect the expression of miR-21 in human esophageal tissues, adjacent tissues, and an esophageal cancer cell line (TE-13). The antisense miR-21 oligonucleotide was generated commercially using the solidphase chemical synthesis method. Transient transfection was used to transfect esophageal cancer cells (TE-13 antisense and TE-13 control cells). Flow cytometry and Transwell cell assays were used to detect the apoptosis and invasion of esophageal cancer cells, respectively. The western blot method was used to detect the expression of PTEN, PDCD4, and K-ras proteins. These analyses determined that mir-21 expression significantly increased in esophageal cancer tissues and in TE-13 cells, and that this phenomenon was not associated with staging or lymph node metastasis. The apoptosis rate of TE-13 control cells was lower than that of antisense TE-13 cells indicating an enhanced 8811 miR-21 in esophageal cancer ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (3): 8810-8818 (2015) invasive ability. In tissues adjacent to esophageal cancer and in TE-13 antisense cells, the expression of PTEN and PDCD4 was found to be higher than that in the control group, whereas the expression of K-ras showed the opposite pattern. Together, these results suggest that miR-21 might be involved in the development and metastasis of esophageal cancer, through interaction with its PDCD4 and K-ras target genes.

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Section: Discussionmentioning

confidence: 99%

Characterization and effects of miR-21 expression in esophageal cancer

et al. 2015

Genet. Mol. Res.

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“…Accumulating evidence indicates that numerous molecular changes are associated with EC tumorigenesis, including epidermal growth factor receptor (EGFR) amplification, phosphoinositide 3-kinase, catalytic subunit alpha (PIK3CA) amplification and mutation (8)(9)(10), and phosphatase and tensin homolog (PTEN) mutation or loss (11,12). Alteration of these molecular events contributes to downstream pathway activation (8)(9)(10)(11)(12).…”

Section: Introductionmentioning

confidence: 99%

“…Alteration of these molecular events contributes to downstream pathway activation (8)(9)(10)(11)(12). The phosphoinositide 3-kinase (PI3K)/AKT and mitogen-activated protein kinase kinase (MEK)/ERK signaling pathways are two important pathways that can be activated by EGFR amplification and PTEN loss, which may ultimately lead to tumorigenesis (13).…”

Section: Introductionmentioning

confidence: 99%

Aloe-emodin suppresses esophageal cancer cell TE1 proliferation by inhibiting AKT and ERK phosphorylation

et al. 2016

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Abstract. Aberrant AKT and extracellular signal-regulated kinase (ERK) activation is often observed in various human cancers. Both AKT and ERK are important in the phosphoinositide 3-kinase/AKT and mitogen-activated protein kinase kinase/ERK signaling pathways, which play vital roles in cell proliferation, differentiation and survival. Compounds that are able to block these pathways have therefore a promising use in cancer treatment and prevention. The present study revealed that AKT and ERK are activated in esophageal cancer TE1 cells. Aloe-emodin, an anthraquinone present in aloe latex, can suppress TE1 cell proliferation and anchor-independent cell growth. Aloe-emodin can also reduce the number of TE1 cells in S phase. Protein analysis indicated that aloe-emodin inhibits the phosphorylation of AKT and ERK in a dose-dependent manner. Overall, the present data indicate that aloe-emodin can suppress TE1 cell growth by inhibiting AKT and ERK phosphorylation, and suggest its clinical use for cancer therapy.

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“…3), which indicated that PTEN had no activity in these cell lines. On the other hand, PTEN protein had high expression in EC9706-pcDNA3.1-wPTEN cells we screened and kept previously, 9 but it had no obvious expression in EC9706 and EC9706-pcDNA3.1 cells (Fig. 4) (P < 0.001), which indicated that EC9706-pcDNA3.1-wPTEN cells could still express PTEN stably.…”

Section: Expression Of Pten and P-pten In Escc Cells And Ec9706 Cellsmentioning

confidence: 93%

“…PTEN can inhibit the activation of Akt, which implicates in cell proliferation and resistance to apoptosis. 5 But PTEN often loses activity because its mutation, phosphorylation, or hyper-methylation in many human cancers, including ESCC, [6][7][8][9][10] and accordingly results in activating of Akt and mTOR. Rapamycin (rapa), and its analogs can inhibit the activity of mTOR by binding with mTOR and interfere the interaction of mTOR with other target proteins in the pathway, and thus targeting mTOR pathway can be a new strategy for the treatment of malignancies.…”

Section: Introductionmentioning

confidence: 99%

Wild-type phosphatase and tensin homolog deleted on chromosome 10 improved the sensitivity of cells to rapamycin through regulating phosphorylation of Akt in esophageal squamous cell carcinoma

Wang

Zheng

et al. 2016

Dis Esophagus

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Esophageal squamous cell carcinoma (ESCC) is one of the most frequently diagnosed cancers in China, but the etiology and mode of carcinogenesis of this disease remain poorly understood. Phosphatase and tensin homolog deleted on chromosome 10 (PTEN), as a negative regulator of Akt/mTOR pathway, frequently mutates or is inactive in many cancers. Although mTOR has been thought a promising cancer therapeutic target, the sensitivity of tumor cells to rapamycin was still to be revaluated. In this study, we measured the effects of rapamycin on cell proliferation and phosphorylation of Akt in ESCC cells with varying degrees of differentiation. And then, the relationship between PTEN status and the sensitivity of cells to rapamycin was investigated in EC9706 cells with or without wild-type PTEN in vitro and in vivo. The results demonstrated ESCC cells with poor differentiation were insensitive to rapamycin of high concentration and rapamycin obviously promoted the phosphorylation of Akt in these cells, but it had no obvious effects on p-Akt in cells with well differentiation. Also, we showed that wild-type PTEN improved the sensitivity of poor differentiation cells to rapamycin through inhibiting phosphorylation of Akt in vitro and in vivo. This study explored the possible molecular mechanism of some ESCC cells insensitive to rapamycin and provided a measure for treating ESCC patients with PTEN inactivation using mTOR inhibitors.

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Mutational Analysis of the PTEN Gene and Its Effects in Esophageal Squamous Cell Carcinoma

Abstract: The findings of the present study demonstrate that there are mutations in the PTEN gene of the ESCC cells and that the wild type PTEN gene has important effects on the ESCC cells in vitro and in vivo.

Cited by 11 publications

References 30 publications

Characterization and effects of miR-21 expression in esophageal cancer

Characterization and effects of miR-21 expression in esophageal cancer

Aloe-emodin suppresses esophageal cancer cell TE1 proliferation by inhibiting AKT and ERK phosphorylation

Wild-type phosphatase and tensin homolog deleted on chromosome 10 improved the sensitivity of cells to rapamycin through regulating phosphorylation of Akt in esophageal squamous cell carcinoma

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