Evidence map›Paper›PMID 38679999›Full record

ArticleAsian Pacific journal of cancer prevention : APJCP2024

LncRNA ANRIL Promotes Glucose Metabolism and Proliferation of Colon Cancer in a High-Glucose Environment and is Associated with Worse Outcome in Diabetic Colon Cancer Patients.

Hala Mosaad, Sally M Shalaby, Nevertety M Mahmoud, Mona M Ahmed, Alaa Fayed, Hassan R Ashour, Walaa Sarhan

Abstract read
In one paragraph

Article in Asian Pacific journal of cancer prevention : APJCP, 2024. 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
–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

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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.

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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

7 authors.

Hala MosaadMedical Biochemistry Department, Faculty of Medicine, Zagazig University, Zagazig, Egypt.
Sally M ShalabyMedical Biochemistry Department, Faculty of Medicine, Zagazig University, Zagazig, Egypt.ORCID 0000-0002-2868-020X
Nevertety M MahmoudClinical Pharmacology Department, Faculty of Medicine, Zagazig University, Zagazig, Egypt.
Mona M AhmedPathology Department, Faculty of Medicine, Zagazig University, Zagazig, Egypt.
Alaa FayedClinical Oncology Department, Faculty of Medicine, Zagazig University, Zagazig, Egypt.
Hassan R AshourDepartment, Faculty of Medicine, Zagazig University, Zagazig, Egypt.
Walaa SarhanMedical Biochemistry Department, Faculty of Medicine, Zagazig University, Zagazig, Egypt.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe potential involvement of type 2 diabetes mellitus (T2DM) as a risk factor for colon cancer (CC) has been previously reported. Epigenetic changes, such as deregulation of long non-coding RNA (lncRNA) and microRNA (miR), have been linked to the advancement of CC; however, the effects of high glucose levels on their deregulation and, in turn, colon cancer remain unexplored.

methodsFifty patients had a dual diagnosis of CC and T2DM, and 60 patients with CC without diabetes mellitus were included in the study. qRT-PCR was used to examine the expression of lncRNA ANRIL and miR-186-5p in tissue samples. ANRIL, miR-186-5p, and their downstream target genes HIF-1α, PFK, HK, Bcl-2, and Bax were also determined in CC cell lines under various glucose conditions. Glucose uptake, lactate production and cells proliferation were estimated in CC cell lines.

resultsA significant upregulation of ANRIL expression levels (p<0.001) and a significant downregulation of miR-186-5p expression (p<0.001) in diabetic colon cancer specimens compared to those in non-diabetic colon cancer group were observed. MiR-186-5p expression levels were inversely correlated with ANRIL expression levels, blood glucose levels and HbA1c%. Concerning in vitro model, a significant upregulation of ANRIL, downregulation of miR-186-5p, upregulation of HIF-1α, glycolytic enzymes and activation of antiapoptotic pathway was detected in higher glucose concentrations than lower one. There was a significant increase of glucose uptake, lactate accumulation and proliferation of the Caco2 and SW620 cell lines in a dose dependent manner of glucose concentrations. Moreover, a significant positive correlation between glucose uptake and ANRIL expression was shown.

conclusionsA high-glucose environment can increase the tumor-promoting effect of ANRIL. ANRIL can promote glucose metabolism and colon cancer proliferation by downregulating miR-186-5p with subsequent upregulation of glycolysis enzymes expression and inhibition of apoptosis.

Indexed as

Cell ProliferationColonic NeoplasmsDiabetes Mellitus, Type 2GlucoseMicroRNAsRNA, Long NoncodingAgedApoptosisBiomarkers, TumorCase-Control StudiesFemaleFollow-Up StudiesGene Expression Regulation, NeoplasticHumansMaleMiddle AgedBiomarkers, TumorCDKN2B antisense RNA, humanGlucoseMicroRNAsMIRN186 microRNA, humanRNA, Long NoncodingANRILColon cancerGlycolysismiR-186-5pType 2 DM

Identifiers

PMID38679999
PMCPMC11162718

What Socratic holds

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Registered trials

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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.