Related Experiment Video
Updated: Mar 7, 2026
07:23
Describing a Transcription Factor Dependent Regulation of the MicroRNA Transcriptome
Published on: June 15, 2016
9.0K
Calcium Dysregulation Promotes Glioma Progression by Inhibiting STAT3 Degradation Through Blocking Chaperone-Mediated
Jialong Chen1, Yixi Lai1, Mingque Li1
1Dongguan Key Laboratory of Environmental Medicine, the First Dongguan Affiliated Hospital, School of Public Health, Guangdong Medical University, Dongguan, China.
Journal of Cellular and Molecular Medicine
|March 5, 2026
Summary
Transient Receptor Potential Canonical 1 (TRPC1) promotes glioma cell migration by stabilizing Signal Transduction and Transcription Activator 3 (STAT3) protein levels. This TRPC1-HDAC6 pathway inhibits STAT3 degradation by suppressing chaperone-mediated autophagy, offering a potential therapeutic target for glioma.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Calcium dysregulation is linked to cancer progression, affecting cell proliferation, migration, and invasion.
- Transient Receptor Potential Canonical 1 (TRPC1) is crucial for calcium homeostasis, but its role in glioma calcium dysregulation is unclear.
Purpose of the Study:
- To investigate the role of TRPC1 in glioma cell migration and its underlying molecular mechanisms.
- To elucidate the relationship between TRPC1, Signal Transduction and Transcription Activator 3 (STAT3), and chaperone-mediated autophagy (CMA) in glioma.
Main Methods:
- Investigated TRPC1's effect on glioma cell migration and STAT3 protein levels.
- Assessed TRPC1's influence on STAT3 stability and CMA activity.
- Examined the interaction between TRPC1, HDAC6, and Heat Shock Cognate 70 in regulating intracellular calcium.
Main Results:
- TRPC1 promotes glioma cell migration by increasing STAT3 protein levels.
- TRPC1 inhibits STAT3 degradation by suppressing CMA activity, identifying STAT3 as a CMA substrate.
- TRPC1 modulates the HDAC6-Heat Shock Cognate 70 interaction via intracellular calcium, impacting CMA and preventing STAT3 degradation.
Conclusions:
- The TRPC1-HDAC6 axis promotes glioma progression by stabilizing STAT3 through the inhibition of CMA.
- Targeting the TRPC1-HDAC6-STAT3-CMA pathway presents a potential therapeutic strategy for glioma treatment.
More Related Videos
Related Concept Videos
01:30Ligand-Gated Ion Channel Receptor: Gating Mechanism
4.4K
Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...
4.4K
03:03mTOR Signaling and Cancer Progression
5.0K
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...
5.0K
01:16Calmodulin-dependent Signaling
6.8K
Calmodulin (CaM) is a calcium-binding protein in eukaryotes that controls various calcium-regulated cellular processes. It has four calcium-binding sites that bind calcium to form the calcium-calmodulin ( Ca2+-CaM) complex. GPCR stimulation increases the calcium levels in the cells that bind to CaM and induces a conformational change.
The Ca2+-CaM complex does not have enzymatic activity by itself. Instead, the complex binds downstream target proteins, including membrane proteins or enzymes,...
The Ca2+-CaM complex does not have enzymatic activity by itself. Instead, the complex binds downstream target proteins, including membrane proteins or enzymes,...
6.8K
01:20The JAK-STAT Signaling Pathway
13.5K
Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as SH2...
13.5K
01:22PI3K/mTOR/AKT Signaling Pathway
6.0K
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...
6.0K
02:23Abnormal Proliferation
5.3K
Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
5.3K