ArticleDNA repair2014
5-Fluorouracil mediated anti-cancer activity in colon cancer cells is through the induction of Adenomatous Polyposis Coli: Implication of the long-patch base excision repair pathway.
Article in DNA repair, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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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.
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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
23 citing papers in PubMed, 50 citations in OpenAlex.
- A Hybrid Bioprinting-Microfabrication Approach to Controllable Multitype Spheroid Arrays for Modeling Tumor Heterogeneity.Advanced healthcare materials · 2026Article
- DiffInvex identifies evolutionary shifts in driver gene repertoires during tumorigenesis and chemotherapy.Nature communications · 2025Article
- Acquired resistance to molecularly targeted therapies for cancer.Cancer drug resistance (Alhambra, Calif.) · 2025Review
- Mechanism of APC truncation involved in colorectal cancer tumorigenesis (Review).Oncology letters · 2025Review
- A panorama of colon cancer in the era of liquid biopsy.The journal of liquid biopsy · 2024Review
- Talazoparib enhances the quinacrine-mediated apoptosis in patient-derived oral mucosa CSCs by inhibiting BER pathway through the modulation of GCN5 and P300.Medical oncology (Northwood, London, England) · 2023Article
- Assessment of the Influence of 5-Fluorouracil on SMAD4 and TGFB1 Gene Expression, Apoptosis Induction and DNA Damage in Human Cell Lines.Bioengineering (Basel, Switzerland) · 2023Article
- Combination of talazoparib and olaparib enhanced the curcumin-mediated apoptosis in oral cancer cells by PARP-1 trapping.Journal of cancer research and clinical oncology · 2022Article
- A Quassinoid Diterpenoid Eurycomanone fromMolecules (Basel, Switzerland) · 2022Article
- Predicting Agents That Can Overcome 5-FU Resistance in Colorectal Cancers via Pharmacogenomic Analysis.Biomedicines · 2021Article
- A Novel Strategy Conjugating PD-L1 Polypeptide With Doxorubicin Alleviates Chemotherapeutic Resistance and Enhances Immune Response in Colon Cancer.Frontiers in oncology · 2021Article
- Dehydroxyhispolon Methyl Ether, A Hispolon Derivative, Inhibits WNT/β-Catenin Signaling to Elicit Human Colorectal Carcinoma Cell Apoptosis.International journal of molecular sciences · 2020Article
- Wnt-Independent and Wnt-Dependent Effects of APC Loss on the Chemotherapeutic Response.International journal of molecular sciences · 2020Review
- Inhibition of the ATR kinase enhances 5-FU sensitivity independently of nonhomologous end-joining and homologous recombination repair pathways.The Journal of biological chemistry · 2020Article
- Overexpression of lamin B1 induces mitotic catastrophe in colon cancer LoVo cells and is associated with worse clinical outcomes.International journal of oncology · 2018Article
- Multiple Roles of APC and its Therapeutic Implications in Colorectal Cancer.Journal of the National Cancer Institute · 2017Review
- How does inflammation drive mutagenesis in colorectal cancer?Trends in cancer research · 2017Article
- Genomic profiling of stage II and III colon cancers reveals APC mutations to be associated with survival in stage III colon cancer patients.Oncotarget · 2016Article
- Interaction between APC and Fen1 during breast carcinogenesis.DNA repair · 2016Review
- Nanoquinacrine induced apoptosis in cervical cancer stem cells through the inhibition of hedgehog-GLI1 cascade: Role of GLI-1.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Colorectal cancer (CRC) patients with APC mutations do not benefit from 5-FU therapy. It was reported that APC physically interacts with POLβ and FEN1, thus blocking LP-BER via APC's DNA repair inhibitory (DRI) domain in vitro. The aim of this study was to elucidate how APC status affects BER and the response of CRC to 5-FU. HCT-116, HT-29, and LOVO cells varying in APC status were treated with 5-FU to evaluate expression, repair, and survival responses. HCT-116 expresses wild-type APC; HT-29 expresses an APC mutant that contains DRI domain; LOVO expresses an APC mutant lacking DRI domain. 5-FU increased the expression of APC and decreased the expression of FEN1 in HCT-116 and HT-29 cells, which were sensitized to 5-FU when compared to LOVO cells. Knockdown of APC in HCT-116 rendered cells resistant to 5-FU, and FEN1 levels remained unchanged. Re-expression of full-length APC in LOVO cells caused sensitivity to 5-FU, and decreased expression of FEN1. These knockdown and addback studies confirmed that the DRI domain is necessary for the APC-mediated reduction in LP-BER and 5-FU. Modelling studies showed that 5-FU can interact with the DRI domain of APC via hydrogen bonding and hydrophobic interactions. 5-FU resistance in CRC occurs with mutations in APC that disrupt or eliminate the DRI domain's interaction with LP-BER. Understanding the type of APC mutation should better predict 5-FU resistance in CRC than simply characterizing APC status as wild-type or mutant.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.