ArticleAmerican journal of physiology. Cell physiology2014
Autocrine regulation of glioma cell proliferation via pHe-sensitive K(+) channels.
Article in American journal of physiology. Cell physiology, 2014. 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
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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, 10 citations in OpenAlex.
- Potassium Channels, Glucose Metabolism and Glycosylation in Cancer Cells.International journal of molecular sciences · 2023Review
- pH-Channeling in Cancer: How pH-Dependence of Cation Channels Shapes Cancer Pathophysiology.Cancers · 2020Review
- Role of endolysosomes and pH in the pathogenesis and treatment of glioblastoma.Cancer reports (Hoboken, N.J.) · 2019Article
- Importance of measuring endolysosome, cytosolic, and extracellular pH in understanding the pathogenesis of and possible treatments for glioblastoma multiforme.Cancer reports (Hoboken, N.J.) · 2019Article
- Quiescence status of glioblastoma stem-like cells involves remodelling of CaScientific reports · 2018Article
- CaFrontiers in molecular neuroscience · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Since the seminal studies of Otto Warburg in the 1920s, it has been widely recognized that cancers grow glycolytically, even in the presence of oxygen. This generates an abundance of protons in a gradient across most solid tumors with an acidic core and an alkaline rim. Whether and how this proton gradient may also serve in an autocrine fashion in these tumors is unclear. We demonstrate that human glioma cells form spheroids that act as a viable three-dimensional tumor model, forming physiologically relevant extracellular pH (pHe) and cell proliferation gradients. Using fluorescent cell cycle trackers, we determined that the rate of cell proliferation is directly dependent on pHe and that cells adjust their growth rate according to their position within the pH gradient. We further show that glioma cells sense pH via H(+)-sensitive K(+) channels, which translate changes in pH into changes in membrane voltage. These channels are tonically active and blocked by acidic pHe, quinine, and ruthenium red. Blockade of this K(+) conductance by acidic pHe or drug inhibition depolarized glioma cells and tumor spheroids and prevented their passage through the hyperpolarization-dependent G1-to-S phase cell cycle checkpoint, thereby inhibiting cell division. In this way, pHe directly determines the proliferative state of glioma cells.
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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.