Evidence mapPaperPMID 41787243Full record

ArticleJournal of cellular and molecular medicine2026

Calcium Dysregulation Promotes Glioma Progression by Inhibiting STAT3 Degradation Through Blocking Chaperone-Mediated Autophagy.

Jialong Chen, Yixi Lai, Mingque Li, ZiWei Cai, Renjian Lu, Linhua Liu, Yongming Peng, Chunlai Fu, Zhefan Xie, Xueqion Zhou and 2 more

Abstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. Article
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

12 authors.

Jialong ChenDongguan Key Laboratory of Environmental Medicine, the First Dongguan Affiliated Hospital, School of Public Health, Guangdong Medical University, Dongguan, China.ORCID https://orcid.org/0000-0001-5040-0692
Yixi LaiDongguan Key Laboratory of Environmental Medicine, the First Dongguan Affiliated Hospital, School of Public Health, Guangdong Medical University, Dongguan, China.
Mingque LiDongguan Key Laboratory of Environmental Medicine, the First Dongguan Affiliated Hospital, School of Public Health, Guangdong Medical University, Dongguan, China.
ZiWei CaiDongguan Key Laboratory of Environmental Medicine, the First Dongguan Affiliated Hospital, School of Public Health, Guangdong Medical University, Dongguan, China.
Renjian LuDongguan Key Laboratory of Environmental Medicine, the First Dongguan Affiliated Hospital, School of Public Health, Guangdong Medical University, Dongguan, China.
Linhua LiuDongguan Key Laboratory of Environmental Medicine, the First Dongguan Affiliated Hospital, School of Public Health, Guangdong Medical University, Dongguan, China.
Yongming PengDongguan Key Laboratory of Environmental Medicine, the First Dongguan Affiliated Hospital, School of Public Health, Guangdong Medical University, Dongguan, China.
Chunlai FuDepartment of Emergency Intensive Care Unit, Affiliated Dongguan People's Hospital, Southern Medical University, Dongguan, Guangdong, People's Republic of China.
Zhefan XieDepartment of Emergency Intensive Care Unit, Affiliated Dongguan People's Hospital, Southern Medical University, Dongguan, Guangdong, People's Republic of China.
Xueqion ZhouDepartment of Occupational Health and Occupational Medicine, School of Public Health, Southern Medical University, Guangzhou, Guangdong Province, China.
Jiaxian LiuDongguan Key Laboratory of Environmental Medicine, the First Dongguan Affiliated Hospital, School of Public Health, Guangdong Medical University, Dongguan, China.
He ZhangDongguan Key Laboratory of Environmental Medicine, the First Dongguan Affiliated Hospital, School of Public Health, Guangdong Medical University, Dongguan, China.

Funding

Basic and Applied Basic Research Foundation of Guangdong Province 2021B1515140032 2022A1515110272 2022A1515140173Discipline Construction Project of Guangdong Medical University 4SG21021GDongguan Social Development Science and Technology (Key) Project 20211800905332Guangdong Medical University Clinical + Basic Medical Science and Technology Innovation Special Program GDMULCJC2024152 GDMULCJC2024153 GDMULCJC2024140National Natural Science Foundation of China 82103879Science Foundation of traditional Chinese medicine administration of Guangdong Province 20222104
6 · The paper itself

Abstract

Calcium dysregulation is closely associated with cancer cell proliferation, migration, and invasion. Transient receptor potential canonical 1 (TRPC1) plays an essential role in regulating calcium homeostasis. However, the role of TRPC1 in calcium dysregulation in gliomas remains incompletely understood. In this study, we demonstrate that TRPC1 promotes glioma cell migration by increasing Signal transduction and transcription activator 3 (STAT3) protein levels. Furthermore, we show that TRPC1 modulates STAT3 stability by inhibiting chaperone-mediated autophagy (CMA), and we identify STAT3 as a novel substrate of CMA. Additionally, TRPC1 modulates the interaction between HDAC6 and Heat Shock Cognate 70 through intracellular Ca

Indexed as

CalciumChaperone-Mediated AutophagyGliomaSTAT3 Transcription FactorAnimalsAutophagyCell Line, TumorCell MovementCell ProliferationDisease ProgressionGene Expression Regulation, NeoplasticHistone Deacetylase 6HumansProteolysisSignal TransductionTRPC Cation ChannelsCalciumHDAC6 protein, humanHistone Deacetylase 6STAT3 protein, humanSTAT3 Transcription Factortransient receptor potential cation channel, subfamily C, member 1TRPC Cation ChannelsCMAgliomaSTAT3TRPC1

Identifiers

PMID41787243
PMCPMC12963025

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.