ArticleCell cycle (Georgetown, Tex.)2020
LncRNA MACC1-AS1/MACC1 enhances the progression of glioma via regulating metabolic plasticity.
Article in Cell cycle (Georgetown, Tex.), 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 It has been retracted, and should not be counted.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 5 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
5 citing papers in PubMed, 9 citations in OpenAlex.
- Glycolysis-associated lncRNAs in cancer energy metabolism and immune microenvironment: a magic key.Frontiers in immunology · 2024Review
- IFN-γ affects pancreatic cancer properties by MACC1-AS1/MACC1 axis via AKT/mTOR signaling pathway.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022Article
- Non-coding RNAs and glioblastoma: Insight into their roles in metastasis.Molecular therapy oncolytics · 2022Review
- Mechanisms of Long Non-Coding RNAs in Biological Characteristics and Aerobic Glycolysis of Glioma.International journal of molecular sciences · 2021Review
- Review
Corrections and comments
- Retraction · 2021-10-11Error in Data · Investigation by Journal/Publisher · Investigation by Third Party · Original Data and/or Images not Provided and/or not Available · Paper Mill · Unreliable Image ·
- Retracted
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study plans to investigate the effects of long-noncoding RNA MACC1-AS1 on glioma cells and its mechanism at metabolic plasticity angle. The MACC1-AS1 level was identified both in glioma tissues and in cells. Then the effects of MACC1-AS1 abnormal level on cell viability, apoptosis, the expression of apoptosis associated protein, glucose metabolism and redox status were measured in A172 and U251 cells by different methods. Furthermore, the interaction of MACC1-AS1 and MACC1 in glioma cells was investigated and the role of AMPK pathway was specifically examined. Our results demonstrated that MACC1-AS1 level was high in glioma tissues and cells, and MACC1-AS1 overexpression was closely associated with poor prognosis of glioma. Notably, under glucose deprivation, the MACC1-AS1 level was significantly increased, and overexpression of MACC1-AS1 increased cell viability but inhibited apoptosis. Also, MACC1-AS1 overexpression obviously increased the levels of GLUT1, HK2, G6PD, MCT1, ATP, lactate and NAPDH as well as promoted the activities of HK2 and LDHA, while reduced ROS level and the ratio of NADP+/NAPDH. In particular, the effects of proliferation, apoptosis and metabolic plasticity of glioma cells caused by MACC1-AS1 overexpression were achieved by positively regulating MACC1, and MACC1-AS1 promoted MACC1 expression via the AMPK pathway. In conclusions, the MACC1-AS1/MACC1 axis exertes the tumor-promoting effect by regulating glucose metabolism and redox homeostasis in glioma cells by activating the AMPK signals.
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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.