ArticleCancer science2014
Krüppel-like factor 8 contributes to hypoxia-induced MDR in gastric cancer cells.
Article in Cancer science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 32 citations in OpenAlex.
- Review
- The hypoxia-inducible factor-1α in stemness and resistance to chemotherapy in gastric cancer: Future directions for therapeutic targeting.Frontiers in cell and developmental biology · 2023Review
- CircSAMD4A contributes to cell doxorubicin resistance in osteosarcoma by regulating the miR-218-5p/KLF8 axis.Open life sciences · 2020Article
- Shedding New Light on Cancer Metabolism: A Metabolic Tightrope Between Life and Death.Frontiers in oncology · 2020Review
- KLF8 is associated with poor prognosis and regulates glycolysis by targeting GLUT4 in gastric cancer.Journal of cellular and molecular medicine · 2019Article
- Mechanisms of Metastasis and Cell Mobility - The Role of Metabolism.Geburtshilfe und Frauenheilkunde · 2019Article
- Berberine Reverses Hypoxia-induced Chemoresistance in Breast Cancer through the Inhibition of AMPK- HIF-1α.International journal of biological sciences · 2017Article
- KLF16 promotes proliferation in gastric cancer cells via regulating p21 and CDK4.American journal of translational research · 2017Article
- Hurdles in selection process of nanodelivery systems for multidrug-resistant cancer.Journal of cancer research and clinical oncology · 2016Review
- Targeting hypoxic response for cancer therapy.Oncotarget · 2016Review
- Role of cancer-associated fibroblasts in invasion and metastasis of gastric cancer.World journal of gastroenterology · 2015Review
- Hypoxia-inducible factors in cancer stem cells and inflammation.Trends in pharmacological sciences · 2015Review
- Induction of cellular prion protein (PrPc) under hypoxia inhibits apoptosis caused by TRAIL treatment.Oncotarget · 2015Article
- Up-regulation of KLF17 expression increases the sensitivity of gastric cancer to 5-fluorouracil.International journal of immunopathology and pharmacologyArticle
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We previously reported that hypoxia-induced MDR in gastric cancer (GC) cells is hypoxia-inducible factor-1 (HIF-1)-dependent. However, the exact mechanisms are still unknown. Our previous study revealed that Krüppel-like factor 8 (KLF8), a novel transcription factor, was associated with malignant phenotype in GC cells. KLF8 is overexpressed in clear cell renal carcinoma lacking von Hippel-Lindau protein function, which resulted in HIF-1 stabilization. Given this association, we hypothesized that KLF8 contributed to hypoxia-induced MDR in GC cells. Initial experiments revealed that hypoxia could increase KLF8 and HIF-1α expressions in GC cells, and KLF8 levels in GC drug-resistant cell lines were higher than in parental cell lines. Subsequent experiments showed that in normoxia, exogenous KLF8 could promote the MDR phenotype; however, blocking KLF8 expression could effectively reverse the MDR phenotype induced by hypoxia. Overexpressed KLF8 increased resistance-associated gene MDR1 mRNA levels, Bcl-2 and P-gp protein levels, and decreased Bax and caspase-3 protein levels in GC cells, and knockout KLF8 reversed these effects. Dual luciferase reporter and ChIP assays showed that KLF8 could promote MDR1 transcriptional activity by combining with KLF8 binding sites located in the upstream of MDR1 transcriptional start site. These results suggest that KLF8 is involved in hypoxia-induced MDR through inhibiting apoptosis and increasing the drug release rate by directly regulating MDR1 transcription.
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