ArticleTranslational oncology2020
Silencing of CHFR Sensitizes Gastric Carcinoma to PARP Inhibitor Treatment.
Article in Translational oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- PARP inhibitors in gastric cancer: unlocking precision oncology.The oncologist · 2025Review
- CENPE and LDHA were potential prognostic biomarkers of chromophobe renal cell carcinoma.European journal of medical research · 2023Article
- Review
- Association between eight hypermethylation-related genes and gastric cancer: a systematic review and meta-analysis.Translational cancer research · 2022Article
- CHFR and Paclitaxel Sensitivity of Ovarian Cancer.Cancers · 2021Article
- Deciphering CHFR Role in Pancreatic Ductal Adenocarcinoma.Frontiers in medicine · 2021Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CHFR is a tumor suppressor that not only recognizes poly(ADP-ribosylation) (PARylation) signals at the sites of DNA damage but also is downregulated in many types of cancer. However, the underlying mechanism linking its role in PARylation-mediated DNA damage repair and tumor suppression is unclear. Here, we examined a panel of gastric cancer cell lines as well as primary tissue samples from gastric cancer patients, and found that CHFR expression was silenced by DNA hypermethylation in gastric cancer including 38.46% of primary gastric cancers. DNMT1 was associated with aberrant methylation of CHFR, and the expression of CHFR was restored by DNMT1 inhibitor 5-aza-2-deoxycytidine (5-aza-CdR) treatment. Moreover, we found that loss of CHFR abolished DNA damage repair and sensitized gastric tumor cells to PARP inhibitor treatment. Thus, our study reveals a potential therapeutic approach for treating gastric cancer with PARP inhibitor and lacking CHFR can serve as a biomarker for predicting the efficacy of PARP inhibitor on the gastric tumor treatment in future.
Identifiers
What OpenQuestion holds
Registered trials
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