ArticleBreast cancer (Tokyo, Japan)2022
LncRNA SNHG5 promotes the glycolysis and proliferation of breast cancer cell through regulating BACH1 via targeting miR-299.
Article in Breast cancer (Tokyo, Japan), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- SNHG5 enhances colorectal cancer metastasis through RNA-protein interaction with GNB2 and activation of canonical Wnt signaling.Non-coding RNA research · 2026Article
- MLWNNR: LncRNA-Disease Association Prediction with Multi-Kernel Learning-Driven Weighted Nuclear Norm Regularization.Interdisciplinary sciences, computational life sciences · 2025Article
- Paeonol regulates glycolytic metabolism by downregulating BACH1 to ameliorate stemness, angiogenesis, and EMT in SiHa cervical cancer cells.Histology and histopathology · 2025Article
- Long noncoding RNAWorld journal of gastrointestinal oncology · 2025Article
- The Multifaceted Roles of BACH1 in Disease: Implications for Biological Functions and Therapeutic Applications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Navigating heme pathways: the breach of heme oxygenase and hemin in breast cancer.Molecular and cellular biochemistry · 2025Review
- The multiple functions and mechanisms of long non-coding RNAs in regulating breast cancer progression.Frontiers in pharmacology · 2025Review
- SNHG12 downregulation induces follicular dysplasia by modulating the glycolysis of granulosa cell in polycystic ovary syndrome.Frontiers in cell and developmental biology · 2025Article
- Article
- Metabolism-regulating non-coding RNAs in breast cancer: roles, mechanisms and clinical applications.Journal of biomedical science · 2024Review
- Transcription factor BACH1 in cancer: roles, mechanisms, and prospects for targeted therapy.Biomarker research · 2024Review
- Glycolysis-associated lncRNAs in cancer energy metabolism and immune microenvironment: a magic key.Frontiers in immunology · 2024Review
- Non-coding RNAs in breast cancer: with a focus on glucose metabolism reprogramming.Discover oncology · 2023Review
- Prognostic Worth of Nrf2/BACH1/HO-1 Protein Expression in the Development of Breast Cancer.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2023Article
- The dual role and mutual dependence of heme/HO-1/Bach1 axis in the carcinogenic and anti-carcinogenic intersection.Journal of cancer research and clinical oncology · 2023Review
- Long non-coding RNAs affecting cell metabolism in cancer.Biology direct · 2022Review
- A lactate-related LncRNA model for predicting prognosis, immune landscape and therapeutic response in breast cancer.Frontiers in genetics · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundBreast cancer (BC) is one of the most common malignant tumors in women. Accumulating studies have been reported that long non-coding RNA (lncRNA) SNHG5 is highly expressed in BC. However, the specific molecular mechanism of SNHG5 in BC is unclear.
methodsGene and protein expressions in BC cell were detected by qRT-PCR and western blotting. The proliferation and cell cycle were measured using colony formation assay and flow cytometry analysis, separately. The glucose consumption and lactate production were determined by using the glucose assay kit and lactate assay kit. A dual-luciferase reporter assay was performed to measure the interaction between miR-299 and SNHG5 or BACH1.
resultsSNHG5 and BACH1 expressions were increased in BC cell while miR-299 level was decreased. SNHG5 increased BACH1 expression by directly targeting miR-299. SNHG5 silencing or miR-299 overexpression suppressed the proliferation of BC cell, arrested the cell cycle in the G1 cell phase, and decreased the glucose consumption and lactate production of BC cell. However, inhibition of miR-299 or overexpression of BACH1 could reverse the inhibitory effects of sh-SNHG5 on cell proliferation and glycolysis in BC.
conclusionSNHG5 promoted the BC cell growth and glycolysis through up-regulating BACH1 expression via targeting miR-299. These findings may improve the diagnostic and therapeutic approaches to BC.
Indexed as
Identifiers
What OpenQuestion holds
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.