Evidence map›Paper›PMID 32016455›Full record

ArticleMolecular medicine reports2020

Long non‑coding RNA BCYRN1 promotes glycolysis and tumor progression by regulating the miR‑149/PKM2 axis in non‑small‑cell lung cancer.

Ning Lang, Chunyang Wang, Jiangyang Zhao, Feng Shi, Tong Wu, Hongyan Cao

RetractedOpen access · bronzeAbstract readRetracted Publication
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.0field-weighted citation impact, top 7% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

31 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Emerging Roles of ncRNAs Regulating PKM2 in Cancer Progression.Current pharmaceutical biotechnology · 2025
    Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. The Role of PKM2 in Diabetic Microangiopathy.Diabetes, metabolic syndrome and obesity : targets and therapy · 2022
    Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Ning LangDepartment of Preventive Health, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.
Chunyang WangDepartment of Thoracic Surgery, First Hospital of Qiqihar City, Qiqihar, Heilongjiang 161000, P.R. China.
Jiangyang ZhaoDepartment of Thoracic Surgery, First Hospital of Qiqihar City, Qiqihar, Heilongjiang 161000, P.R. China.
Feng ShiDepartment of Respiratory Diseases, First Hospital of Qiqihar City, Qiqihar, Heilongjiang 161000, P.R. China.
Tong WuDepartment of Respiratory Diseases, First Hospital of Qiqihar City, Qiqihar, Heilongjiang 161000, P.R. China.
Hongyan CaoDepartment of Oncology, First Hospital of Qiqihar City, Qiqihar, Heilongjiang 161000, P.R. China.
Qiqihar Medical University · CNHarbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer cells use aerobic glycolysis to sustain their proliferation. Long non‑coding RNA brain cytoplasmic RNA 1 (BCYRN1) has been reported to act as an oncogene in non‑small‑cell lung cancer (NSCLC). The present study investigated the role of BCYRN1 in NSCLC glycolysis. BCYRN1 expression was detected in NSCLC cells and tissues using reverse transcription‑quantitative PCR. The effect of BCYRN1 on aerobic glycolysis was examined by measuring NSCLC cell glucose catabolism and lactate synthesis. The relationships between BCYRN1 and microRNA (miR)‑149, and between miR‑149 and pyruvate kinase M1/2 (PKM2) were measured using a dual‑luciferase reporter assay. Cell proliferation and invasion were analyzed by the Cell Counting kit‑8 assay and the Matrigel invasion assay, respectively. High BCYRN1 expression was observed in NSCLC tissues and cells compared with the corresponding controls. BCYRN1 induced glycolysis and upregulated the expression levels of PKM2 in NSCLC cells. In addition, BCYRN1 regulated miR‑149 expression levels, and miR‑149 inhibitor rescued the effects of si‑BCYRN1 on glucose consumption and lactate production. miR‑149 knockdown significantly enhanced the expression of PKM2. Furthermore, PKM2 inhibition significantly reversed the effects of miR‑149 inhibitor on glucose catabolism and lactate synthesis. Furthermore, PKM2 was involved in NSCLC cell proliferation and invasion, and BCYRN1 knockdown and miR‑149 overexpression inhibited both processes. The present study suggested that BCYRN1 was involved in cell glycolysis, proliferation and invasion during NSCLC via regulating miR‑149 and PKM2.

Indexed as

Gene Expression Regulation, Neoplastic3' Untranslated RegionsAdultCarcinoma, Non-Small-Cell LungCarrier ProteinsCell Line, TumorDisease ProgressionFemaleGenes, ReporterGlycolysisHumansLung NeoplasmsMaleMembrane ProteinsMicroRNAsMiddle Aged3' Untranslated RegionsCarrier Proteinslong non-coding RNA BC200, humanMembrane ProteinsMicroRNAsMIRN149 microRNA, humanRNA, Long NoncodingThyroid Hormone-Binding ProteinsThyroid Hormonesbrain cytoplasmic rna 1glycolysismicrorna-149non-small-cell lung cancerpyruvate kinase M1/2

Identifiers

PMID32016455
PMCPMC7003037
OpenAlexW2999032275

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

None linked

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.