ArticleMolecular medicine reports2017
Effect of RNA interference of the expression of HMGA2 on the proliferation and invasion ability of ACHN renal cell carcinoma cells.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Effect of the antifungal drug ciclopirox on the inhibition of HMGA2-mediated oncogenic capacity in ACHN renal cell carcinoma.Frontiers in pharmacology · 2026Article
- The emerging role and mechanism of HMGA2 in breast cancer.Journal of cancer research and clinical oncology · 2024Review
- Effects of HMGA2 on the epithelial-mesenchymal transition-related genes in ACHN renal cell carcinoma cells-derived xenografts in nude mice.BMC cancer · 2022Article
- Effects ofThe Journal of international medical research · 2022Article
- NUF2 Drives Clear Cell Renal Cell Carcinoma by Activating HMGA2 Transcription through KDM2A-mediated H3K36me2 Demethylation.International journal of biological sciences · 2022Article
- Let‑7a‑5p may participate in the pathogenesis of diabetic nephropathy through targeting HMGA2.Molecular medicine reports · 2019Article
- miR-1-3p suppresses the epithelial-mesenchymal transition property in renal cell cancer by downregulating Fibronectin 1.Cancer management and research · 2019Article
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8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This aim of the present study was to observe the effect of high mobility group AT‑hook 2 (HMGA2) on the proliferation and invasion ability of ACHN renal cell carcinoma (RCC) cells. Human ACHN cells, an RCC cell line, and HKC normal human renal tubular epithelial cells were cultured. HMGA2 small interfering (si)RNA, Mock‑siRNA and their negative control group were designed and synthesized. Subsequently, the ACHN cells were transiently transfected using RNA interference technology. Finally, the mRNA and protein expression levels of HMGA2 were detected using reverse transcription-polymerase chain reaction and western blot analyses. The proliferation ability of the ACHN cells was determined using MTT, and ACHN cell invasion ability was detected using the Transwell method. The results showed that the mRNA and protein expression levels of HMGA2 in the ACHN cells were considerably higher, compared with those in the HKC cells (P<0.01). The RCC cells, in which the expression of HMGA2 was specifically silenced, was successfully constructed. The proliferation rate of cells in the HMGA2‑siRNA group was significantly lower, compared with that of cells in the Mock‑siRNA group and control group at 24, 48, 72 and 96 h post‑transfection (P<0.05). The invasion ability of cells in the HMGA2‑siRNA group was significantly lower, compared with that of cells in the Mock‑siRNA group and control group (P<0.05) 48 h following transfection. Therefore, the HMGA2 gene may function as an oncogene in the occurrence and development of RCC, and provide specific targets for the targeted therapy of RCC. Further detailed investigations of the HMGA2 gene are important for future gene therapy of RCC.
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