ArticleMolecular genetics & genomic medicine2019
Forkhead box O3 promotes colon cancer proliferation and drug resistance by activating MDR1 expression.
Article in Molecular genetics & genomic medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- The Role of Noncoding RNAs in the Prognosis and Diagnosis of Colorectal Cancer: An Emerging Biomarker.MicroRNA (Shariqah, United Arab Emirates) · 2026Review
- Article
- CircRNAs in colorectal cancer: potential roles, clinical applications, and natural product-based regulation.Frontiers in oncology · 2025Review
- Review
- Mechanism of multidrug resistance to chemotherapy mediated by P‑glycoprotein (Review).International journal of oncology · 2023Review
- Forkhead Box Transcription Factors: Double-Edged Swords in Cancer.Cancer research · 2022Review
- How Dysregulated Ion Channels and Transporters Take a Hand in Esophageal, Liver, and Colorectal Cancer.Reviews of physiology, biochemistry and pharmacology · 2021Review
- Prediction of genome-wide effects of single nucleotide variants on transcription factor binding.Scientific reports · 2020Article
- Serum Circular FoxO3a Serves as a Novel Prognostic Biomarker in Squamous Cervical Cancer.Cancer management and research · 2020Article
- The emerging role of microRNAs and long noncoding RNAs in drug resistance of hepatocellular carcinoma.Molecular cancer · 2019Review
- Forkhead box O3 promotes colon cancer proliferation and drug resistance by activating MDR1 expression.Molecular genetics & genomic medicine · 2019Article
- Long non-coding RNA ZEB2-AS1 promotes proliferation and inhibits apoptosis of colon cancer cells via miR-143/bcl-2 axis.American journal of translational research · 2019Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGlobally, colon cancer (CC) is the third reason of tumor-related deaths. Previous reports indicate that Forkhead box O3 (FOXO3) is involved in the development of various tumors and may have different effects depending upon the types of tumors. Hence, this study was to examine the effects of FOXO3 on CC cells and uncover the possible mechanisms.
methodsMTT and cell count assay were applied to analyze the viability of transfected CC cells. rVista, dual luciferase reporter assay, and chromatin immunoprecipitation assay were used to identify the downstream target of FOXO3 in HCT116 cells. The mRNA and protein abundance of FOXO3 and MDR1 were determined by quantitative PCR and Western blot, respectively.
resultsForkhead box O3 stimulated the proliferation of both HCT116 and DLD1 cells. Moreover, FOXO3 overexpression inhibited doxorubicin sensitivity of HCT116 cells, while the knockout of FOXO3 by FOXO3 shRNA restored the doxorubicin sensitivity in doxorubicin-resistant HCT116 DR cells. Next, we found that FOXO3 directly bound to the promoter of MDR1 and enhanced MDR1 expression in HCT116 cells. MDR1 overexpression enhanced the viability and doxorubicin resistance of CC cells. Besides, MDR1 overexpression plasmid significantly abrogated the decrease in cell proliferation and resistance of HCT116 cells to doxorubicin caused by FOXO3 knockout.
conclusionForkhead box O3 exhibited promotive effects on the proliferation and doxorubicin resistance in CC cells via targeting MDR1.
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