Evidence map›Paper›PMID 37926998›Full record

ArticleTechnology in cancer research & treatment

SGMS1-AS1/MicroRNA-106a-5p/CPT2 Axis as a Novel Target for Regulating Lactate Metabolism in Colon Cancer.

Yan Ruochen, Ji Wenbin, Gao Chao, Yuan Yuhua, Qi Feng

Open access · goldAbstract read
In one paragraph

Article in Technology in cancer research & treatment. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.5field-weighted citation impact, top 26% 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

3 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. Article
  3. 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

5 authors at 1 institution in 1 country.

Yan RuochenDepartment of Clinical Laboratory, Tianjin Medical University General Hospital, Tianjin, P.R. China.
Ji WenbinDepartment of General Surgery, Tianjin Medical University General Hospital, Tianjin, P.R. China.ORCID 0000-0003-4160-089X
Gao ChaoDepartment of General Surgery, Tianjin Medical University General Hospital, Tianjin, P.R. China.ORCID 0000-0001-9083-6706
Yuan YuhuaClinical Laboratory Diagnostics, Tianjin Medical University General Hospital Airport Site, Tianjin, P.R. China.
Qi FengDepartment of General Surgery, Tianjin Medical University General Hospital, Tianjin, P.R. China.
Tianjin Medical University General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeThe malignant transformation of cells can lead to aerobic glycolysis, an important form of metabolic reprogramming in colon cancer cells, which can cause the accumulation of lactate and accelerate the proliferation of tumor cells also enhance their chemotherapy drug resistance. The aim of this study was to investigate the possible molecular mechanisms responsible for the increased lactate expression in colon cancer.

methodsSeveral bioinformatics methods, including differential analysis, gene ontology enrichment, univariate and multivariate Cox regression analysis were used to find the lactic acid-related gene carnitine palmitoyltransferase 2. We analyzed the relationship between carnitine palmitoyltransferase 2 and clinical features as well as immune microenvironment. To further explore the mechanism of carnitine palmitoyltransferase 2 in colon cancer, we performed methylation analysis and constructed a competitive endogenous RNA network, which was validated in cell lines and clinical specimens.

resultsWe used bioinformatics to select the lactic acid-related gene carnitine palmitoyltransferase 2 and found low expression of carnitine palmitoyltransferase 2 was associated with poor prognosis in colon cancer. An inhibitory tumor microenvironment was created when carnitine palmitoyltransferase 2 expression was reduced, with decreased CD4 T cells, CD8 T cells, dendritic cells, and B cells but increased cancer-associated fibroblasts. Methylation analysis showed that the abnormal decrease in carnitine palmitoyltransferase 2 might be caused by hypermethylation. We constructed a network of SGMS1-AS1/microRNA-106a-5p/carnitine palmitoyltransferase 2 and verified their expression in cell lines and clinical specimens.

conclusionOur work revealed the possible mechanism of lactate accumulation in colon cancer and explored a new potential treatment for colon cancer by cutting off aerobic glycolysis in tumor cells.

Indexed as

Carnitine O-PalmitoyltransferaseColonic NeoplasmsMicroRNAsCell Transformation, NeoplasticHumansLactic AcidMembrane ProteinsNerve Tissue ProteinsTransferases (Other Substituted Phosphate Groups)Tumor MicroenvironmentCarnitine O-PalmitoyltransferaseLactic AcidMembrane ProteinsMicroRNAsMIRN106 microRNA, humanNerve Tissue ProteinsSGMS1 protein, humanTransferases (Other Substituted Phosphate Groups)ceRNAcolon cancerglycolysislactatemetabolic reprogramming

Identifiers

PMID37926998
PMCPMC10629329
OpenAlexW4388423913

What OpenQuestion holds

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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.