Evidence map›Paper›PMID 34658120›Full record

ArticleCell biology international2022

Long noncoding RNA HAGLR sponges miR-338-3p to promote 5-Fu resistance in gastric cancer through targeting the LDHA-glycolysis pathway.

Jing Hu, Lujie Huang, Qi Ding, Jiaming Lv, Zhe Chen

Open access · hybridAbstract read
In one paragraph

Article in Cell biology international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.9field-weighted citation impact, top 7% 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

33 citing papers in PubMed, 41 citations in OpenAlex.

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  12. Long noncoding HOXD-AS1: a crucial regulator of malignancy.Frontiers in cell and developmental biology · 2025
    Review
  13. Article
  14. siRNA-based strategies to combat drug resistance in gastric cancer.Medical oncology (Northwood, London, England) · 2024
    Review
  15. Article
  16. Article
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  19. Review
  20. Soft Tissue Ewing Sarcoma Cell Drug Resistance Revisited: A Systems Biology Approach.International journal of environmental research and public health · 2023
    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

5 authors at 1 institution in 1 country.

Jing HuDepartment of Radiation Oncology, Ningbo Medical Center Lihuili Hospital, Ningbo, Zhejiang, China.
Lujie HuangDepartment of General Practice, Ningbo Medical Center Lihuili Hospital, Ningbo, Zhejiang, China.
Qi DingDepartment of Histopathology, Ningbo Diagnostic Pathology Center, Ningbo, Zhejiang, China.
Jiaming LvDepartment of Radiation Oncology, Ningbo Medical Center Lihuili Hospital, Ningbo, Zhejiang, China.
Zhe ChenDepartment of Cardiothoracic Surgery, Ningbo Medical Center Lihuili Hospital, Ningbo, Zhejiang, China.ORCID http://orcid.org/0000-0001-8885-3179
Ningbo Medical Center Lihuili Hospital · CN

Funding

Ningbo Natural Science Foundation 2021J293
6 · The paper itself

Abstract

Gastric cancer (GC) is one of the most common human malignancies due to its invasiveness and metastasis. 5-Fu is a widely applied chemotherapeutic agent against GC. Although 5-Fu therapy has achieved improvements in GC treatment, a large fraction of patients developed drug resistance which significantly limited its clinical applications. Recent studies revealed the pivotal roles of long noncoding RNAs (lncRNAs) in tumorigenesis and progressions of various tumors, including GC. However, the biological roles and molecular mechanisms of lncRNA HAGLR in GC remain unclear. Here, we report HAGLR was upregulated in both GC tissues and cell lines. In addition, HAGLR was associated with a poorly survival rate of GC patients. Blocking HAGLR inhibited GC cells proliferation and sensitized GC cells to 5-Fu. Bioinformatical analysis and luciferase assay demonstrated that HAGLR sponged microRNA (miR)-338-3p, which functions as a tumor suppressor in GC to downregulate its expressions. Moreover, from the established 5-Fu resistant GC cell line (HGC27 5-Fu R), we detected significantly elevated HAGLR, downregulated miR-338-3p, and glucose metabolism compared with parental HGC27 cells. We identified lactate dehydrogenase-A (LDHA), a glucose metabolism key enzyme, was the direct target of miR-338-3p in GC cells. Rescue experiments demonstrated that restoration of miR-338-3p in HAGLR-overexpressing HGC27 5-Fu R cells successfully overrode the HAGLR-promoted 5-Fu resistance through targeting LDHA. Taken together, this study revealed essential roles and molecular mechanisms for the HAGLR-mediated 5-Fu resistance in GC, contributing to the development of new noncoding RNA-based therapeutic strategies against chemoresistant GC.

Indexed as

MicroRNAsRNA, Long NoncodingStomach NeoplasmsCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticGlycolysisHumansLactate Dehydrogenase 5Lactate Dehydrogenase 5MicroRNAsMIRN338 microRNA, humanRNA, Long Noncodingchemoresistancegastric cancerglucose metabolismLDHAlncRNA HAGLRWarburg effect

Identifiers

PMID34658120
PMCPMC9300138
OpenAlexW3205225726

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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 OpenQuestion graph.