ArticleCell death & disease2019
miR-23b-3p suppressing PGC1α promotes proliferation through reprogramming metabolism in osteosarcoma.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
29 citing papers in PubMed, 58 citations in OpenAlex.
- MiR-1293 modulates PPARGC1A to promote proliferation and metastasis of oral carcinoma cells.Journal of molecular histology · 2025Article
- Article
- RFWD3 Reprograms Nucleotide Metabolism Through PHGDH to Induce Chemoresistance In Osteosarcoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Construction and evaluation of a prognostic model based on the expression of the metabolism-related signatures in patients with osteosarcoma.BMC musculoskeletal disorders · 2025Article
- Follicular fluid extracellular vesicles improve bovine oocyte quality via lipid and mitochondrial modulation.Frontiers in veterinary science · 2025Article
- The Oncogenic Role ofInternational journal of molecular sciences · 2024Article
- LncRNA RPARP-AS1 promotes the progression of osteosarcoma cells through regulating lipid metabolism.BMC cancer · 2024Article
- RCOR1 is targeted by miR-23b-3p to modulate growth, colony formation, migration, and invasion of prostate cancer cells.International journal of clinical and experimental pathology · 2024Article
- Icariin Attenuates Human Renal Tubular Epithelial Cell Senescence by Targeting PAK2Current pharmaceutical biotechnology · 2024Article
- Overexpression of HSPB6 inhibits osteosarcoma progress through the ERK signaling pathway.Clinical and experimental medicine · 2023Article
- Nano-Based Drug Delivery Systems: Potential Developments in the Therapy of Metastatic Osteosarcoma-A Narrative Review.Pharmaceutics · 2023Review
- Mitochondria Deregulations in Cancer Offer Several Potential Targets of Therapeutic Interventions.International journal of molecular sciences · 2023Review
- APOC1 promotes the progression of osteosarcoma by binding to MTCH2.Experimental and therapeutic medicine · 2023Article
- Molecular mechanisms of osteosarcoma metastasis and possible treatment opportunities.Frontiers in oncology · 2023Review
- Silencing of circCYP51A1 represses cell progression and glycolysis by regulating miR-490-3p/KLF12 axis in osteosarcoma under hypoxia.Journal of bone oncology · 2022Article
- Article
- Targeting PGC1α to wrestle cancer: a compelling therapeutic opportunity.Journal of cancer research and clinical oncology · 2022Review
- Ailanthone Inhibits Proliferation, Migration and Invasion of Osteosarcoma Cells by Downregulating the Serine Biosynthetic Pathway.Frontiers in oncology · 2022Article
- Inhibition of miR-23b-3p Ameliorates Scar-Like Phenotypes of Keloid Fibroblasts by Facilitating A20 Expression.Clinical, cosmetic and investigational dermatology · 2022Article
- The roles of glycolysis in osteosarcoma.Frontiers in pharmacology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metabolic shift from oxidative phosphorylation (OXPHOS) to glycolysis is a hallmark of osteosarcoma (OS). However, the mechanisms of the metabolic switch have not been completely elucidated. Here we reported that the miR-23b-3p was significantly upregulated in OS cells. Functional studies suggested that knockdown of miR-23b-3p could inhibit OS cell proliferation in vitro or in vivo. In addition, suppression of miR-23b-3p could lead to upregulation of OXPHOS and suppression of glycolysis. Mechanistically, miR-23b-3p promoted OS cell proliferation and inhibited OXPHOS in OS, at least in part, by directly targeting peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC1α) and inhibiting its expression. Our data highlights important roles of miR-23b-3p and PGC1α in glucose metabolism reprogram of OS. The suppression of miR-23b-3p may provide effective therapeutic strategies for the treatment of OS.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.