ArticleRSC advances2018
Knockdown of UCA1 inhibits viability and glycolysis by suppressing PKM2 expression through the mTOR pathway in non-small cell lung cancer cells.
Article in RSC advances, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 8 citations in OpenAlex.
- LncRMRP drives bladder cancer invasion via a lactylation-driven positive feedback circuit.Oncogene · 2026Article
- The role and application prospects of glycolysis-related non-coding RNAs in lung cancer.Journal of translational medicine · 2026Review
- Research progress on the role of PKM2 in the immune response.Frontiers in immunology · 2022Review
- Long Non-Coding RNAs as Potential Diagnostic and Prognostic Biomarkers in Breast Cancer: Progress and Prospects.Frontiers in oncology · 2021Review
- The Role of Long Non-coding RNAs in Cancer Metabolism: A Concise Review.Frontiers in oncology · 2020Review
- The prognostic value and mechanisms of lncRNA UCA1 in human cancer.Cancer management and research · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
LncRNA urothelial carcinoma associated 1 (UCA1) was reported to be upregulated in non-small cell lung cancer (NSCLC) tissues and contributed to NSCLC progression. Additionally, it has been proposed that the oncogenic role of UCA1 may be related to glucose metabolism in bladder cancer. However, whether and how UCA1 regulates glucose metabolism in the progression of NSCLC remains unknown. Our results showed that knockdown of UCA1 inhibited the viability of NSCLC cells. UCA1 silencing suppressed glycolysis of NSCLC cells by reducing the glucose consumption and lactate production. Additionally, knockdown of UCA1 suppressed PKM2 expression and the mTOR pathway in NSCLC cells. Mechanistically, PKM2 knockdown suppressed the effects of UCA1 on viability and glycolysis of NSCLC cells and inhibition of the mTOR pathway suppressed the effects of UCA1 on viability, glycolysis, and PKM2 expression in NSCLC cells. In conclusion, knockdown of UCA1 inhibited viability and glycolysis by suppressing PKM2 expression maybe through the mTOR pathway in NSCLC cells, providing a novel insight into the molecular mechanism of UCA1 involved in the regulation of glucose metabolism in NSCLC cells.
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.