ArticleOncology reports2019
Dehydrogenase/reductase SDR family member 2 silencing sensitizes an oxaliplatin‑resistant cell line to oxaliplatin by inhibiting excision repair cross‑complementing group 1 protein expression.
Article in Oncology reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 10 citations in OpenAlex.
- CRISPR/Cas9-mediated silencing of CD44: unveiling the role of hyaluronic acid-mediated interactions in cancer drug resistance.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Auxiliary Diagnosis and Prognostic Value of Dehydrogenase/Reductase 2 (DHRS2) in Various Tumors.Iranian journal of public health · 2023Article
- Article
- Molecular Biology of theCells · 2021Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxaliplatin (Oxa)‑based chemotherapy is widely used as the first‑line treatment for colorectal cancer (CRC). However, Oxa‑resistance is common for many postoperative CRC patients. To explore drug resistance in CRC, an Oxa‑resistant cell line, HCT116/Oxa, was established from parental HCT116 cells. These Oxa‑resistant cells exhibited characteristics of epithelial‑mesenchymal transition (EMT) and a higher migratory capacity than parental cells. Protein profiles of HCT116/Oxa and HCT116 cells were compared using a tandem mass tag‑based quantitative proteomics technique. The protein dehydrogenase/reductase SDR family member 2 (DHRS2) was revealed to be highly expressed in HCT116/Oxa cells. Silencing of DHRS2 in HCT116/Oxa cells effectively restored Oxa‑sensitivity by suppressing the expression of excision repair cross‑complementing group 1 protein via a p53‑dependent pathway, and reversed the EMT phenotype. Overall, the suppression of DHRS2 expression may be a promising strategy for the prevention of Oxa‑resistance in CRC.
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Registered trials
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