High level of CFTR expression is associated with tumor aggression and knockdown of CFTR suppresses proliferation of ovarian cancer in vitro and in vivo

Xu, Jiao; Yong, Min; Li, Jia; Dong, Xin; Yu, Tinghe; Fu, Xiao; Hu, Lina

doi:10.3892/or.2015.3829

Cited by 55 publications

(41 citation statements)

References 22 publications

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“…Collectively, these results clearly indicate that low level of CFTR expression is indicative of advanced disease and poor prognosis in NPC. Previous studies from both our groups and others have also shown the correlation of CFTR expression levels and cancer prognosis in different cancers [18–24]. Consistent with the finding in NPC in the present study, we have previously reported that low CFTR expression is correlated with cancer progression and poor prognosis in prostate, breast, colon and lung cancers [18–20, 23].…”

Section: Discussionsupporting

confidence: 92%

CFTR is a potential marker for nasopharyngeal carcinoma prognosis and metastasis

Zhang

et al. 2016

Oncotarget

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While there is an increasing interest in the correlation of cystic fibrosis transmembrane conductance regulator (CFTR) and cancer incidence, the role of CFTR in nasopharyngeal carcinoma (NPC) development remains unknown. In this study, we aimed to explore the prognostic value of CFTR in NPC patients. The expression of CFTR was determined in NPC cell lines and tissues. Statistical analysis was utilized to evaluate the correlation between CFTR expression levels and clinicopathological characteristics and prognosis in 225 cases of NPC patients. The results showed that CFTR was down-regulated in NPC tissues and cell lines. Low expression of CFTR was correlated with advanced stage (p = 0.026), distant metastasis (p < 0.001) and poor prognosis (p < 0.01). Multivariate analysis identified CFTR as an independent prognostic factor (p = 0.003). Additionally, wound healing and transwell assays revealed that overexpression of CFTR inhibited NPC cell migration and invasion, whereas knockdown of CFTR promoted cell migration and invasion. Thus, the current study indicates that CFTR, as demonstrated to play an important role in tumor migration and invasion, may be used as a potential prognostic indicator in NPC.

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Section: Discussionsupporting

confidence: 92%

CFTR is a potential marker for nasopharyngeal carcinoma prognosis and metastasis

Zhang

et al. 2016

Oncotarget

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“…Thus, changes in CFTR function not only appear to have consequences on placental ion and fluid transport but may also contribute to altered trophoblast invasion in preeclampsia. Another example based on experiments with human ovarian carcinoma cells Progress in Understanding Cystic Fibrosis 6 showed that CFTR silencing by RNAi significantly reduced cell migration and invasion under in vitro conditions and that the tumorigenic potential of these cells in vivo was suppressed compared to controls [67]. This result was consistent with the observation that CFTR expression in ovarian cancer was higher relative to normal ovarian epithelial cells or benign ovarian tumors and that enhanced CFTR expression was associated with advanced International Federation of Gynecology and Obstetrics (FIGO) staging and poor histopathology grade.…”

Section: Cftr and Epithelial Wound Repairmentioning

confidence: 99%

CFTR Involvement in Cell Migration and Epithelial Restitution

O’Grady¹

2017

Progress in Understanding Cystic Fibrosis

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Over the past decade, research has shown that cystic fibrosis transmembrane conductance regulator (CFTR) plays an important role in epithelial cell migration and wound healing. Experiments with airway epithelium, ovarian epithelial cells, placental epithelium and epidermal keratinocytes demonstrated that CFTR function is necessary to achieve maximum migration rates during restitution and in certain cancer cells, CFTR activity contributes to tumor cell invasion. Multiple mechanisms appear to underlie the motility-promoting actions of CFTR, and although many details remain to be established, our present understanding indicates that processes such as electrotaxis (galvanotaxis), integrin-mediated cell adhesion and lamellipodia protrusion are dependent on normal CFTR function. In this chapter, the role of CFTR in epithelial cell migration and its implications in cystic fibrosis (CF) will be reviewed with emphasis on the underlying mechanisms that may explain observations made in various epithelial tissues, particularly in airways. Ultimately, a better understanding of CFTR involvement in epithelial repair may lead to new therapeutic approaches to improve barrier function and reduce airway infection and inflammation associated with CF.

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“…Due to hypermethylation of promoter region, the decreased expression of CFTR was proved to be closely correlated with the high malignancy, progression, and poor prognosis. However, the expression of CFTR in ovarian cancer was significantly higher than that in normal ovaries and benign ovarian tumor, indicating that CFTR play an oncogenic role in the pathogenesis of ovarian cancer (Xu et al, ). Esophageal cancer is one of the most deadliest malignancies, while the involvement of CFTR in esophageal cancer still has not been reported.…”

Section: Discussionmentioning

confidence: 99%

CFTR inhibits the invasion and growth of esophageal cancer cells by inhibiting the expression of NF‐κB

Wang

Peng

et al. 2018

Cell Biology International

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Our study aimed to explore the function of cystic fibrosis transmembrane conductance regulator (CFTR) in esophageal cancer. Twenty patients with esophageal squamous cell carcinoma (ESCC) and 20 patients with esophageal adenocarcinoma (EA) were enrolled in this study. The levels of CFTR and NF‐κB in tumor tissues and adjacent normal tissues were detected, respectively. The expression of CFTR were detected by qRT‐PCR and Western blot in normal esophageal cell line, esophagus squamous cell, carcinoma cell lines, and EA cell lines, respectively. Effects of CFTR silencing and overexpression on NF‐κB protein expression were detected by Western blot. Transwell assay was performed to detect cell invasion. Mouse tumor model was established and the effect of CFTR inhibitor on tumor growth was examined. The expression of CFTR was downregulated in tumor tissues and cancer cell lines. CFTR silencing promoted the expression of NF‐κB‐p65 and NF‐κB‐p50, and the results of CFTR overexpression were reversed. In addition, CFTR silencing promoted the invasion of cancer cells and tumor growth in mice. Besides that, NF‐κB inhibitor reduced the enhancing effects of CFTR silencing on esophageal cell invasion. We conclude that CFTR inhibits the growth and migration of esophageal cancer cells by downregulating of the NF‐κB protein expression.

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High level of CFTR expression is associated with tumor aggression and knockdown of CFTR suppresses proliferation of ovarian cancer in vitro and in vivo

Cited by 55 publications

References 22 publications

CFTR is a potential marker for nasopharyngeal carcinoma prognosis and metastasis

CFTR is a potential marker for nasopharyngeal carcinoma prognosis and metastasis

CFTR Involvement in Cell Migration and Epithelial Restitution

CFTR inhibits the invasion and growth of esophageal cancer cells by inhibiting the expression of NF‐κB

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