ArticleMedical science monitor : international medical journal of experimental and clinical research2019
MicroRNA-106a-3p Induces Apatinib Resistance and Activates Janus-Activated Kinase 2 (JAK2)/Signal Transducer and Activator of Transcription 3 (STAT3) by Targeting the SOCS System in Gastric Cancer.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2019. 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, 24 citations in OpenAlex.
- Extracellular vesicles from activated Vδ2 T cells inhibit viral replication and enhance adaptive antiviral immunity.Journal of translational medicine · 2026Article
- Suppressor of cytokine signaling 2 modulates regulatory T cell activity to suppress liver hepatocellular carcinoma growth and metastasis.World journal of gastroenterology · 2025Article
- Silencing suppressor of cytokine signaling 3 induces apoptosis and activates the p-STAT3/NF-κB pathway in hypoxic cultivated H9c2 cells.Journal of physiology and biochemistry · 2024Article
- Dysregulated Signalling Pathways Driving Anticancer Drug Resistance.International journal of molecular sciences · 2023Review
- Oncogenic role of microRNA-19b-3p-mediated SOCS3 in glioma through activation of JAK-STAT pathway.Metabolic brain disease · 2023Article
- SOCS5 contributes to temozolomide resistance in glioblastoma by regulating Bcl-2-mediated autophagy.Bioengineered · 2022Article
- MicroRNA Alterations Induced in Human Skin by Diesel Fumes, Ozone, and UV Radiation.Journal of personalized medicine · 2022Article
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- Up-regulation of SOCS4 promotes cell proliferation and migration in esophageal squamous cell carcinoma.Translational cancer research · 2021Article
- Clinical crosstalk between microRNAs and gastric cancer (Review).International journal of oncology · 2021Review
- Mechanisms of Action And Clinical Implications of MicroRNAs in the Drug Resistance of Gastric Cancer.Frontiers in oncology · 2021Review
- STAT3 Pathway in Gastric Cancer: Signaling, Therapeutic Targeting and Future Prospects.Biology · 2020Review
- Long Non-Coding RNA LINC00239 Functions as a Competitive Endogenous RNA by Sponging microRNA-484 and Enhancing KLF12 Expression to Promote the Oncogenicity of Colorectal Cancer.OncoTargets and therapy · 2020Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND MicroRNA (miR)-106a was involved in the tumorigenesis and highly expressed in gastric cancer. Required apatinib resistance greatly limits its efficacy in patients. Thus, the aim of the present study was to investigate the potential role of miR-106a-3p in gastric cancer cells with apatinib-resistance. MATERIAL AND METHODS The expression of miR-106a-3p was quantified by real-time quantitative polymerase chain reaction (RT-qPCR). Cell Counting Kit-8 (CCK-8) assay was performed to analyze the sensitivity of gastric cancer cells to apatinib. The expression of relevant drug-resistant proteins was detected by western blot. We searched Targetscan6.2 to find out the target gene of miR-106a-3p. Luciferase reporter assay was used to analyze whether miR-106a-3p bound to relevant gene of SOCS family. The SOCS2, SOCS4, and SOCS5 were qualified by western blot, and their mRNA levels were detected by RT-qPCR. Further, JAK2, STAT3, and their phosphorylation levels were detected by western blot. RESULTS The results showed that the expression of miR-106a-3p was increased in apatinib‑resistant gastric cancer, while miR-106a-3p inhibitor reduced the drug-resistance of SGC-7901-AP cells to apatinib. Dual luciferase reporter gene assay suggested that SOCS2, SOCS4, and SOCS5 were target genes of miR-106a-3p. The relevant SOCS genes silencing reversed the effects of miR-106a-3p inhibitor on decreasing the apatinib resistance of SGC-7901-AP cells, while the phosphorylation level of JAK and STAT reduced by miR-106a-3p inhibitor were increased. CONCLUSIONS miR-106a-3p induces apatinib resistance and activates JAK2/STAT3 by targeting SOCS system in gastric cancer. miR-106a-3p/SOCS plays a potent role in gastric cancer cell resistance to apatinib.
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