CHFR gene is neither mutated nor hypermethylated in ovarian cancer

Ludwig, Agnieszka H.; Bujko, Mateusz; Bidziński, Mariusz; Kupryjańczyk, Jolanta

doi:10.1016/j.cdp.2006.04.005

Cited by 6 publications

(4 citation statements)

References 29 publications

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“…Apparently, DNA methylation was not responsible for the expression of the BCSG1 gene. Similar observations have been obtained in cervical cancer and premalignant cervical lesions, for example [24,25,26,27,28], although it is well known that DNA methylation can lead to gene silencing. Some genes were silenced but demethylated, while others were activated but methylated.…”

Section: Discussionsupporting

confidence: 82%

“…The lack of correlation between DNA methylation and gene expression suggested that other mechanisms might be involved in the regulation of gene transcription, e.g. gene mutations or polymorphisms [27], interactions of crucial positive or negative transcription factors [28] and DNA methylation-independent epigenetic events [29]. Reduced gene expression despite promoter hypomethylation may also result from transcriptional suppression through a long-range epigenetic silencing mechanism that affects both methylated and unmethylated physically distant gene clusters [30].…”

Section: Discussionmentioning

confidence: 99%

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BCSG1 Methylation Status and BCSG1 Expression in Breast Tissues Derived from Chinese Women with Breast Cancer

Gu¹,

Tan²,

Lu³

et al. 2008

Oncology

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Objective: To investigate the role of DNA methylation in the regulation of BCSG1 gene expression in breast tissues derived from Chinese women with breast cancer. Methods: The methylation status of exon 1 of the BCSG1 gene in breast cancer, and matched non-neoplastic adjacent and benign lesion tissues was extensively examined using methylation-specific PCR analysis. Corresponding mRNA expression levels were determined by real-time PCR. Results: We found: (1) the BCSG1 gene was universally demethylated in all breast tissues regardless of the tissue state, although 50–60% of the samples displayed methylated products as well; (2) DNA methylation correlated to the expression of the BCSG1 gene in tumor tissues, but not in non-neoplastic adjacent and benign tissues; (3) breast tumor tissues expressed lower BCSG1 than non-neoplastic adjacent tissues. Conclusions: Our data revealed a unique expression pattern and methylation status of the BCSG1 gene in breast tissues derived from Chinese patients and suggested both methylation status and mechanisms underlying BCSG1 regulation might be closely related to the racial background.

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Section: Discussionsupporting

confidence: 82%

Section: Discussionmentioning

confidence: 99%

BCSG1 Methylation Status and BCSG1 Expression in Breast Tissues Derived from Chinese Women with Breast Cancer

Gu¹,

Tan²,

Lu³

et al. 2008

Oncology

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“…For example, nasopharyngeal carcinoma has high frequency of CHFR methylation at 61.1% (22). In contrast, breast cancer has low level of CHFR methylation at 0.9% (23) and ovarian cancer has no methylation (24). CHFR promoter hypermethylation of primary OSCC was 34.7% in our study.…”

Section: Discussionmentioning

confidence: 42%

Aberrant promoter hypermethylation of the CHFR gene in oral squamous cell carcinomas

Baba

Hara²,

Kato³

et al. 2009

Oncol Rep

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Abstract. Recent studies have shown that promoter hypermethylation of tumor suppressor genes is an important factor in carcinogenesis of several human organs. The purpose of this study was to examine the methylation status of CHFR, a novel cell cycle regulatory gene, in both primary oral cancer tumors and the adjacent normal mucosa, and to clarify the relation between the methylation status and expression of the CHFR-related chromosomal passenger protein Aurora-A. The methylation status of the CHFR gene was examined by the methylation-specific PCR (MSP) in 49 primary oral squamous cell carcinomas (OSCC) and 6 OSCC cell lines. In 13 cases, the adjacent normal oral mucosal tissues were also examined. Normal oral mucosa from 18 healthy volunteers was used as the control. The mRNA level of Aurora-A and CHFR in OSCC cell lines was investigated by real-time RT PCR and the protein expression of Aurora-A in certain tumor samples was confirmed by immunohistochemistry. Aberrant promoter methylation of the CHFR gene was detected in 34.7% (17 of 49) of OSCC cases. As for the 13 OSCC cases with paired cancerous and adjacent normal tissues, promoter hypermethylation of the CHFR gene was detected in 46.1% (6 of 13) of the cancerous tissues. In contrast, promoter hypermethylation of the CHFR gene was recognized in only 7.7% (1 of 13) of the surrounding normal mucosa.

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“…Despite this widespread use of taxanes, little is known about CHFR in ovarian cancer. One early study indicated that the CHFR gene is neither methylated nor mutated in ovarian cancer [ 33 ], whereas a subsequent report indicated that the CHFR gene is hypermethylated and downregulated at the mRNA level [ 34 ]. More recently, the deubiquitinase UBC13, acting through its substrate DNMT1, was shown to cause increased methylation of the CHFR locus and diminished CHFR expression [ 35 ].…”

Section: Introductionmentioning

confidence: 99%

CHFR and Paclitaxel Sensitivity of Ovarian Cancer

Hendrickson

Visscher

Hou

et al. 2021

Cancers

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The poly(ADP-ribose) binding protein CHFR regulates cellular responses to mitotic stress. The deubiquitinase UBC13, which regulates CHFR levels, has been associated with better overall survival in paclitaxel-treated ovarian cancer. Despite the extensive use of taxanes in the treatment of ovarian cancer, little is known about expression of CHFR itself in this disease. In the present study, tissue microarrays containing ovarian carcinoma samples from 417 women who underwent initial surgical debulking were stained with anti-CHFR antibody and scored in a blinded fashion. CHFR levels, expressed as a modified H-score, were examined for association with histology, grade, time to progression (TTP) and overall survival (OS). In addition, patient-derived xenografts from 69 ovarian carcinoma patients were examined for CHFR expression and sensitivity to paclitaxel monotherapy. In clinical ovarian cancer specimens, CHFR expression was positively associated with serous histology (p = 0.0048), higher grade (p = 0.000014) and higher stage (p = 0.016). After correction for stage and debulking, there was no significant association between CHFR staining and overall survival (p = 0.62) or time to progression (p = 0.91) in patients with high grade serous cancers treated with platinum/taxane chemotherapy (N = 249). Likewise, no association between CHFR expression and paclitaxel sensitivity was observed in ovarian cancer PDXs treated with paclitaxel monotherapy. Accordingly, differences in CHFR expression are unlikely to play a major role in paclitaxel sensitivity of high grade serous ovarian cancer.

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CHFR gene is neither mutated nor hypermethylated in ovarian cancer

Cited by 6 publications

References 29 publications

BCSG1 Methylation Status and BCSG1 Expression in Breast Tissues Derived from Chinese Women with Breast Cancer

BCSG1 Methylation Status and BCSG1 Expression in Breast Tissues Derived from Chinese Women with Breast Cancer

Aberrant promoter hypermethylation of the CHFR gene in oral squamous cell carcinomas

CHFR and Paclitaxel Sensitivity of Ovarian Cancer

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