Evidence mapPaperPMID 36950803Full record

ArticleJournal of cellular and molecular medicine2023

NR3C2 inhibits the proliferation of colorectal cancer via regulating glucose metabolism and phosphorylating AMPK.

Hui Liu, Wenqi Lei, Zhigui Li, Xiaodong Wang, Liming Zhou

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07087561 (The Effects and Mechanisms of Short-Term Nutritional Enhancement Combined With Health Education on Clinical Outcomes in Postoperative Patients With Colorectal Cancer), which is not on this map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
5.5field-weighted citation impact, top 4% 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.

NCT07087561 narecruitingnot on this mapstarted 2024, after this paper: background citation

The Effects and Mechanisms of Short-Term Nutritional Enhancement Combined With Health Education on Clinical Outcomes in Postoperative Patients With Colorectal Cancer: A Multicenter, Open-Label, Randomized Controlled Trial

TypeinterventionalSponsorXiaoqin LuoRan2024 to 2030Enrolled360ConditionsColorectal Cancer (Diagnosis), Malnutrition or Risk of MalnutritionArmsPersonalized Oral Nutritional Supplementation, Personalized Parenteral Nutritional Supplementation, Structured Nutrition-Focused Health Education
3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 23 citations in OpenAlex.

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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

5 authors at 1 institution in 1 country.

Hui LiuDepartment of Pharmacology, West China School of Basic Science and Forensic Medicine, Sichuan University, Chengdu, China.
Wenqi LeiDepartment of Pharmacology, West China School of Basic Science and Forensic Medicine, Sichuan University, Chengdu, China.
Zhigui LiDepartment of Gastrointestinal Surgery, West China Hospital, Sichuan University, Chengdu, China.ORCID 0000-0002-0936-1131
Xiaodong WangDepartment of Gastrointestinal Surgery, West China Hospital, Sichuan University, Chengdu, China.
Liming ZhouDepartment of Pharmacology, West China School of Basic Science and Forensic Medicine, Sichuan University, Chengdu, China.ORCID 0000-0002-9775-5965
Sichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We aim to investigate the roles and mechanisms of NR3C2 in colorectal cancer (CRC). The expression of NR3C2 in CRC tumours and paired paracancerous tissues of 71 CRC patients and five CRC cell lines was detected by western blotting, immunohistochemistry and real-time reverse-transcription PCR. Moreover, NR3C2 was overexpressed or knocked down in CRC cells by lentiviral vector transfection. The proliferation of cells was measured by MTT, colony formation assay and flow cytometry. Glucose metabolism was assessed by detecting lactate production, glucose consumption and ATP production. Western blotting and real-time reverse-transcription PCR were used to detect the expression of AMPK, LDHA and HK2. The expression of NR3C2 was significantly decreased in CRC tumours compared to paracancerous tissues, which was correlated with distant metastasis, poor prognosis and advanced stages of CRC patients. Overexpressing NR3C2 suppressed the proliferation and promoted the G2/M cell cycle arrest of CRC cells. Furthermore, NR3C2 inhibited glucose metabolism by decreasing the expression of HK2 and LDHA. The phosphorylation of AMPK was also downregulated in CRC cells overexpressing NR3C2. This study demonstrated that NR3C2 inhibited the proliferation of CRC by inhibiting glucose metabolism and phosphorylation of AMPK which may serve as a therapeutic target for CRC.

Indexed as

AMP-Activated Protein KinasesColorectal NeoplasmsReceptors, MineralocorticoidCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticGlucoseHumansAMP-Activated Protein KinasesGlucoseNR3C2 protein, humanReceptors, MineralocorticoidAMPKcolorectal cancerglucose metabolismNR3C2

Identifiers

PMID36950803
PMCPMC10098300
OpenAlexW4360599894

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

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 Socratic graph.