Evidence map›Paper›PMID 24380845›Full record

ArticleAmerican journal of physiology. Cell physiology2014

Autocrine regulation of glioma cell proliferation via pHe-sensitive K(+) channels.

Avinash Honasoge, Katherine A Shelton, Harald Sontheimer

Abstract read
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.3field-weighted citation impact, top 39% 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

6 citing papers in PubMed, 10 citations in OpenAlex.

  1. Potassium Channels, Glucose Metabolism and Glycosylation in Cancer Cells.International journal of molecular sciences · 2023
    Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. CaFrontiers in molecular neuroscience · 2018
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Avinash HonasogeDepartment of Neurobiology and Center for Glial Biology in Medicine, University of Alabama at Birmingham, Birmingham, Alabama.
Katherine A Shelton
Harald Sontheimer
University of Alabama at Birmingham · US

Funding

Virology CoreP30AI027767 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI OLAF KUTSCH · 1988 to 2026
$84.1M
ROS Modulation of Innate and Adaptive Immunity in RAP30AR048311 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MOUNTZ, JOHN D · 2001 to 2017
$9.5M
UAB Neuroscience Core CenterP30NS047466 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI STANDAERT, DAVID G. · 2005 to 2019
$8.5M
The Role of Ion Transport in Glioma Migration, Proliferation, and ApoptosisR01NS036692 · NINDS · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI SONTHEIMER, HARALD W · 1997 to 2024
$6.8M
UAB Research Training Program in Neurobiology of Cognition and Cognitive DisordersT32NS061788 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Farah Dominique Lubin · 2008 to 2026
$4.5M
PROPERTIES AND FUNCTION OF GLIA ION CHANNELSR01NS031234 · NINDS · YALE UNIVERSITY · PI SONTHEIMER, HARALD W · 1994 to 2011
$3.3M
NIAID NIH HHS 3P30 AI-027767-22S1NIAMS NIH HHS 5P30 AR-048311NIAMS NIH HHS P30 AR048311NINDS NIH HHS P30 NS-047466NINDS NIH HHS P30 NS047466NINDS NIH HHS R01 NS-031234NINDS NIH HHS R01 NS-036692NINDS NIH HHS T32 NS061788
6 · The paper itself

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.

Indexed as

Autocrine CommunicationCell ProliferationIon Channel GatingBrain NeoplasmsCell Line, TumorG1 Phase Cell Cycle CheckpointsGliomaHumansHydrogen-Ion ConcentrationKineticsMembrane PotentialsPotassium Channel BlockersPotassium ChannelsSignal TransductionSpheroids, CellularPotassium Channel BlockersPotassium Channelscell cyclegliomapHpotassium channel

Identifiers

PMID24380845
PMCPMC4042621
OpenAlexW2316259413

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.