ArticleMolecular medicine reports2019
miR‑185 regulates the growth of osteosarcoma cells via targeting Hexokinase 2.
Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 22 citations in OpenAlex.
- Metabolic-immune crosstalk in osteosarcoma: mechanisms and therapeutic opportunities.Frontiers in immunology · 2026Review
- miR-10b-5p promotes tumor growth by regulating cell metabolism in liver cancer via targeting SLC38A2.Cancer biology & therapy · 2024Article
- Hypoxia‑regulated exosomal miR‑185 inhibits esophageal squamous cell carcinoma progression and predicts prognosis.Oncology letters · 2024Article
- Reprogramming of glucose metabolism: Metabolic alterations in the progression of osteosarcoma.Journal of bone oncology · 2024Review
- Circ_0000376 regulates miR-577/HK2/LDHA signaling pathway to promote the growth, invasion and glycolysis of osteosarcoma.Journal of orthopaedic surgery and research · 2024Article
- Article
- Functional importance of glucose transporters and chromatin epigenetic factors in Glioblastoma Multiforme (GBM): possible therapeutics.Metabolic brain disease · 2023Review
- Role of microRNAs in glycolysis in gynecological tumors (Review).International journal of oncology · 2023Review
- miRNA-guided reprogramming of glucose and glutamine metabolism and its impact on cell adhesion/migration during solid tumor progression.Cellular and molecular life sciences : CMLS · 2022Review
- Role of miRNA-145, 148, and 185 and Stem Cells in Prostate Cancer.International journal of molecular sciences · 2022Review
- Insight into the interplay between mitochondria-regulated cell death and energetic metabolism in osteosarcoma.Frontiers in cell and developmental biology · 2022Review
- The roles of glycolysis in osteosarcoma.Frontiers in pharmacology · 2022Review
- Epigenetic Small-Molecule Modulators Targeting Metabolic Pathways in Cancer.Sub-cellular biochemistry · 2022Article
- Long non-coding RNA SNHG20 promotes ovarian cancer development by targeting microRNA-338-3p to regulate MCL1 expression.Oncology letters · 2021Article
- Diagnostic Value of Plasma miR-145 and miR-185 as Targeting of the APRIL Oncogene in the B-cell Chronic Lymphocytic Leukemia.Asian Pacific journal of cancer prevention : APJCP · 2021Article
- Role of long intergenic non-protein coding RNA 00152 in pancreatic cancer glycolysisJournal of Cancer · 2021Article
- Regulation of Glycolysis by Non-coding RNAs in Cancer: Switching on the Warburg Effect.Molecular therapy oncolytics · 2020Review
- MiR-503-5p functions as an oncogene in oral squamous cell carcinoma by targeting Smad7.Histology and histopathology · 2020Article
- Ubiquitin-like protein FAT10 promotes osteosarcoma glycolysis and growth by upregulating PFKFB3 via stabilization of EGFR.American journal of cancer research · 2020Article
- Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNAs (miRNAs) have been proposed as potential prognostic and diagnostic biomarkers in numerous types of cancer, including osteosarcoma (OS), which is the most common bone malignancy. The present study revealed that the expression of miR‑185 was downregulated in OS tissues and cells. Overexpression of miR‑185 significantly suppressed the proliferation and migration of OS cells. To further investigate the functional roles of miR‑185 in OS, the downstream targets of miR‑185 were predicted using the microRNA.org database. The results revealed that in cancer cells, hexokinase 2 (HK2), the rate‑limiting enzyme of glycolysis, was a potential target of miR‑185. Molecular analysis indicated that miR‑185 binds to the 3'‑untranslated region of HK2 mRNA. Overexpressed miR‑185 downregulated the mRNA and protein levels of HK2 in OS cells. In addition, an inverse correlation between the expression of miR‑185 and HK2 was reported in OS. Consistent with the downregulation of HK2 induced by miR‑185, overexpression of HK2 in OS cells significantly attenuated the inhibitory effects of miR‑185 on glucose consumption and lactate production, while depletion of miR‑185 promoted the glycolysis of OS cells. Additionally, restoration of HK2 abolished the inhibitory effects of miR‑185 on the proliferation of OS cells. In summary, these results revealed that miR‑185 suppressed the glucose metabolism of OS cells; thus, miR‑185 may be considered as a promising therapeutic target for the treatment of OS.
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