Related Experiment Video
Updated: Jun 25, 2025
06:51
Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer
Published on: July 21, 2018
17.9K
LncARSR promotes glioma tumor growth by mediating glycolysis through the STAT3/HK2 axis
Zhenyang Tian1, Qi Dai2, Bin Liu2
1School of Pharmacy, Hunan Traditional Chinese Medicinal College, Zhuzhou, Hunan, China.
Cytokine
|May 30, 2024
Summary
Long non-coding RNA ARSR (lncARSR) promotes glioma development by enhancing glycolysis. It targets the STAT3-HK2 pathway, increasing proliferation, migration, and invasion in brain tumors.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Glioma is the most common malignant brain tumor.
- Understanding the role of long non-coding RNAs (lncRNAs) in glioma is crucial.
- Glycolysis is a key metabolic pathway implicated in cancer progression.
Purpose of the Study:
- To investigate the role of the glycolysis-related lncRNA, lncARSR, in glioma.
- To elucidate the underlying mechanisms by which lncARSR influences glioma progression.
- To explore the potential therapeutic targeting of the lncARSR-mediated pathway.
Main Methods:
- Assessed lncARSR expression in glioma and normal glial cells.
- Utilized cell-based assays (CCK-8, wound healing, Transwell) to measure proliferation, migration, and invasion.
- Employed flow cytometry for apoptosis and cell cycle analysis.
- Quantified glycolysis indicators and protein expression via biochemical assays and immunoblotting.
- Investigated the STAT3-HK2 interaction using dual-luciferase reporter and ChIP assays.
- Conducted in vivo animal experiments to assess lncARSR's impact on glioma growth.
Main Results:
- lncARSR expression was significantly elevated in glioma cells.
- lncARSR overexpression promoted glioma cell proliferation, migration, invasion, and G2/M phase arrest.
- lncARSR enhanced glycolysis by increasing glucose uptake, lactate production, ATP levels, and key glycolytic enzyme expression (HK2, PFK1, PKM2, GLUT1, LDHA).
- lncARSR knockdown reduced STAT3 binding to the HK2 promoter.
- STAT3 upregulation reversed the inhibitory effects of lncARSR knockdown on glioma progression and glycolysis.
- In vivo, lncARSR knockdown suppressed glioma growth and proliferation markers (Ki67, PCNA).
Conclusions:
- lncARSR acts as an oncogenic lncRNA in glioma.
- lncARSR promotes glioma development and progression by enhancing glycolysis.
- The STAT3-HK2 axis is a key mechanism through which lncARSR exerts its effects in glioma.
Related Concept Videos
03:03mTOR Signaling and Cancer Progression
3.8K
The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
The mTOR pathway or the...
3.8K
01:22PI3K/mTOR/AKT Signaling Pathway
3.5K
The mammalian target of rapamycin (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast, mTORC2 consists of a...
3.5K
02:39lncRNA - Long Non-coding RNAs
8.6K
In humans, more than 80% of the genome gets transcribed. However, only around 2% of the genome codes for proteins. The remaining part produces non-coding RNAs which includes ribosomal RNAs, transfer RNAs, telomerase RNAs, and regulatory RNAs, among other types. A large number of regulatory non-coding RNAs have been classified into two groups depending upon their length – small non-coding RNAs, such as microRNA, which are less than 200 nucleotides in length, and long non-coding RNA...
8.6K
02:53Adaptive Mechanisms in Cancer Cells
5.7K
Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
5.7K