Lower Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) Promotes the Proliferation and Migration of Endometrial Carcinoma

Xia, Xian; Wang, Jie; Liu, Yuan; Yue, Ming

doi:10.12659/msm.899341

Cited by 20 publications

(11 citation statements)

References 34 publications

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“…Considerably higher expression of CFTR in ovarian cancer was seen in vitro and in vivo , so downregulation of CFTR or dysfunctional CFTR should suppress aggressive malignant biological behaviors of ovarian cancer cells [ 22 ]. However, compared with cells from normal endometrium, the expression of CFTR was significantly upregulated in endometrial carcinoma cells, which could result in increased proliferation and transfer of endometrial carcinoma cells [ 23 ]. Due to CFTR dysfunction in the cervix, women with CF have an abnormally thick and dense cervical mucus [ 24 ].…”

Section: Discussionmentioning

confidence: 99%

Malignancies in patients with cystic fibrosis: a case series

et al. 2022

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Background Previous reports have shown an increased number of colorectal cancers in patients with cystic fibrosis. We assessed the database of our cystic fibrosis center to identify patients with all kinds of cancer retrospectively. All patients visiting the Cystic Fibrosis Centre Innsbruck between 1995 and 2019 were included. Case presentation Among 229 patients with cystic fibrosis treated at the Cystic Fibrosis Centre in Innsbruck between 1995 and 2019, 11 subjects were diagnosed with a malignant disease. The median age at diagnosis was 25.2 years (mean 24.3 years). There were four gynecological malignancies (cervical intraepithelial neoplasia and cervical cancer), two hematological malignancies (acute lymphocytic leukemia), one gastrointestinal malignancy (peritoneal mesothelioma), and four malignancies from other origins (malignant melanoma, neuroblastoma, adrenocortical carcinoma, and thyroid cancer). One malignancy occurred after lung transplantation. There was a strong preponderance of females, with 10 of the 11 cases occurring in women. Six deaths were attributed to cancer. Conclusions Most diagnoses were made below 30 years of age, and half of the subjects died from the malignant disease. Awareness of a possible malignancy is needed in patients with atypical symptoms. Regular screenings for cancer should also be considered, not only for gastrointestinal tumors.

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Section: Discussionmentioning

confidence: 99%

Malignancies in patients with cystic fibrosis: a case series

et al. 2022

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“…The results showed that CFTR overexpression suppresses cell proliferation, migration and invasion in CRC. Epithelial-mesenchymal transition (EMT) can inhibit the proliferation and migration ability of endometrial tumor cells, 26,27 and some studies found that EMT can be promoted by inhibiting the expression of CFTR. 16 These results further suggest that CFTR may be a candidate tumor suppressor gene for CRC.…”

Section: Discussionmentioning

confidence: 99%

<p>CFTR Functions as a Tumor Suppressor and Is Regulated by DNA Methylation in Colorectal Cancer</p>

Liu¹,

Song²,

Li³

et al. 2020

CMAR

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Purpose: Cystic fibrosis transmembrane conductance regulator (CFTR) was shown to be downregulated or silenced in carcinomas and acts as a candidate tumor suppressor gene. However, the function of CFTR gene in colorectal cancer (CRC) is still unclear. This aim of this study was to investigate the CFTR promoter methylation status and its impact on the expression and functional role of CFTR in CRC development.Patients and Methods: CFTR expression in CRC tissues and CRC cell lines was detected via quantitative real-time polymerase chain reaction (qRT-PCR) and immunohistochemistry (IHC). The promoter methylation status of CFTR was measured using methylation-specific PCR (MSP). colony formation, transwell, and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays were used to evaluate the effect of CFTR overexpression in CRC cell lines. Results: qRT-PCR and IHC results indicated that CFTR expression was downregulated in the CRC tissues compared to the adjacent normal tissues. The promoter methylation status of CFTR was further analyzed in 70 CRC specimens. MSP validation showed methylation of CFTR promoter in 62.2% (45/70) of CRC tissues. The methylation of CFTR promoter was significantly associated with age (P=0.013) and lymph node metastasis (P=0.026) in CRC tissues. Results of transwell, MTT, and colony formation assays showed that CFTR overexpression inhibited the migration, invasion, and proliferation of CRC cells. Conclusion: CFTR expression was downregulated in CRC and promoter methylation may be responsible for this downregulation. Overexpression of CFTR may suppress CRC tumor growth by inhibiting the proliferation, migration, and invasion of CRC cells. CFTR promoter methylation was significantly correlated with lymph node metastasis; thus, CFTR may be a potential marker for lymph node metastasis of CRC.

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“…CFTR , a cAMP-activated chloride channel widely distributed in the epithelial cells of various tissues (28), plays an important role in maintaining cell homeostasis and is associated with metabolism (29). Mutations in CFTR are responsible for regulation of epithelial ion and water transport and fluid homeostasis, which affects the epithelial tissue of various organ systems, including the urogenital, respiratory and gastrointestinal systems (30).…”

Section: Discussionmentioning

confidence: 99%

Identification of CFTR as a novel key gene in chromophobe renal cell carcinoma through bioinformatics analysis

Wang

Chai

2019

Oncol Lett

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Chromophobe renal cell carcinoma (chRCC), the third most common histological subtype of RCC, comprises 5–7% of all RCC cases. The aim of the present study was to identify potential biomarkers for chRCC and to examine the underlying mechanisms. A total of 4 profile datasets were downloaded from the Gene Expression Omnibus database to identify differentially expressed genes (DEGs). Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses of DEGs were performed with the Database for Annotation, Visualization and Integrated Discovery. A protein-protein interaction (PPI) network was constructed to predict hub genes. Hub gene expression within chRCC across multiple datasets, as well as overall survival, were investigated by utilizing the Oncomine platform and UALCAN dataset, separately. A total of 266 DEGs (88 upregulated genes and 168 downregulated genes) were identified from 4 profile datasets. Integrating the results from the PPI network, Oncomine platform and survival analysis, CFTR was screened as a key factor in the prognosis of chRCC. GO and KEGG analysis revealed that 266 DEGs were mainly enriched in 17 terms and 9 pathways. The present study identified key genes and potential molecular mechanisms underlying the development of chRCC, and CFTR may be a potential prognostic biomarker and novel therapeutic target for chRCC.

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Lower Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) Promotes the Proliferation and Migration of Endometrial Carcinoma

Cited by 20 publications

References 34 publications

Malignancies in patients with cystic fibrosis: a case series

Malignancies in patients with cystic fibrosis: a case series

<p>CFTR Functions as a Tumor Suppressor and Is Regulated by DNA Methylation in Colorectal Cancer</p>

Identification of CFTR as a novel key gene in chromophobe renal cell carcinoma through bioinformatics analysis

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