ArticleOncoTargets and therapy2020
MiR-138 Suppresses the PDK1 Expression to Decrease the Oxaliplatin Resistance of Colorectal Cancer.
Article in OncoTargets and therapy, 2020. 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, 50 citations in OpenAlex.
- HNF1A-AS1 promotes oral squamous cell carcinoma progression via regulating miR-138/CDK6 pathway.Odontology · 2025Article
- Prostate cancer cells elevate glycolysis and G6PD in response to caffeic acid phenethyl ester-induced growth inhibition.BMC cancer · 2025Article
- The Role of miR-138 in Cardiovascular Diseases.BioMed research international · 2025Review
- The role of glycolysis in tumorigenesis: From biological aspects to therapeutic opportunities.Neoplasia (New York, N.Y.) · 2024Review
- FOXA1/MND1/TKT axis regulates gastric cancer progression and oxaliplatin sensitivity via PI3K/AKT signaling pathway.Cancer cell international · 2023Article
- In vitro siRNA-mediated GPX4 and AKT1 silencing in oxaliplatin resistance cancer cells induces ferroptosis and apoptosis.Medical oncology (Northwood, London, England) · 2023Article
- miR-138-5p targets MCU to inhibit mitochondrial biogenesis and colorectal cancer growth.Journal of cellular and molecular medicine · 2023Article
- Warburg effect in colorectal cancer: the emerging roles in tumor microenvironment and therapeutic implications.Journal of hematology & oncology · 2022Review
- Atractylenolide I inhibited the development of malignant colorectal cancer cells and enhanced oxaliplatin sensitivity through the PDK1-FoxO1 axis.Journal of gastrointestinal oncology · 2022Article
- Comparative Study of Autophagy in Oxaliplatin-Sensitive and Resistant SNU-C5 Colon Cancer Cells.Biomolecules & therapeutics · 2022Article
- Lnc-RP11-536 K7.3/SOX2/HIF-1α signaling axis regulates oxaliplatin resistance in patient-derived colorectal cancer organoids.Journal of experimental & clinical cancer research : CR · 2021Article
- Glycolysis-induced drug resistance in tumors-A response to danger signals?Neoplasia (New York, N.Y.) · 2021Review
- Tumour Microenvironment: Roles of the Aryl Hydrocarbon Receptor, O-GlcNAcylation, Acetyl-CoA and Melatonergic Pathway in Regulating Dynamic Metabolic Interactions across Cell Types-Tumour Microenvironment and Metabolism.International journal of molecular sciences · 2020Review
- The Role of microRNAs in Regulating Cancer Cell Response to Oxaliplatin-Containing Regimens.Technology in cancer research & treatmentReview
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundOxaliplatin is one kind of platinum-based drug. It is effective and commonly used in the treatment of colorectal cancer (CRC). However, development of acquired drug resistance is still a big obstacle during the oxaliplatin therapy. It is urgent to take strategies to decrease the oxaliplatin resistance of CRC. MATERIALS AND
methodsOxaliplatin-resistant HT29 and SW480 (HT29/R and SW480/R) cells were acquired through long-term exposure to oxaliplatin by using the routine HT29 and SW480 cells. Relative glucose consumption, lactate generation and LDH activity were tested to evaluate the glycolysis of CRC cell lines. MTT assays were conducted to evaluate the differences of oxaliplatin sensitivity between HT29/R (SW480/R) cells and their parental HT29 (SW480) cells. Regulation of miR-138 on PDK1 was confirmed through qRT-PCR, Western blot and dual-luciferase reporter assays. Reactive oxygen species (ROS) levels were measured by flow cytometry.
resultsHT29/R and SW480/R cells exhibited higher glucose consumption, lactate production and LDH activity compared to their parental HT29 and SW480 cells. However, oxygen consumption rate (OCR) in HT29/R and SW480/R cells is lower than that in HT29 and SW480 cells, respectively. Results of MTT assays showed that treatment with miR-138 can increase the cytotoxicity of oxaliplatin to HT29/R and SW480/R cells. Research on mechanisms showed that PDK1 was the target of miR-138. Overexpression of miR-138 can inhibit the expression of PDK1, and thus increase the OCR of HT29/R and SW480/R cells. Under the treatment of oxaliplatin, the miR-138-overexpressed HT29/R and SW480/R cells generated more amount of ROS to get into the apoptosis process.
conclusionOverexpression of miR-138 suppressed the PDK1 expression to decrease the oxaliplatin resistance of CRC.
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