Evidence map›Paper›PMID 25078450›Full record

ArticleMolecules and cells2014

A long non-coding RNA snaR contributes to 5-fluorouracil resistance in human colon cancer cells.

Heejin Lee, Chongtae Kim, Ja-Lok Ku, Wook Kim, Sungjoo Kim Yoon, Hyo-Jeong Kuh, Jeong-Hwa Lee, Suk Woo Nam, Eun Kyung Lee

Open access · diamondAbstract read
In one paragraph

Article in Molecules and cells, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

48 citing papers in PubMed, 86 citations in OpenAlex.

  1. Review
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  4. Apelin/APJ: Another Player in the Cancer Biology Network.International journal of molecular sciences · 2025
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  20. The emerging role of noncoding RNAs in colorectal cancer chemoresistance.Cellular oncology (Dordrecht, Netherlands) · 2019
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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

9 authors at 3 institutions in 1 country.

Heejin LeeDepartment of Biochemistry, College of Medicine, Catholic University of Korea, Seoul 137-701, Korea.
Chongtae KimDepartment of Biochemistry, College of Medicine, Catholic University of Korea, Seoul 137-701, Korea.
Ja-Lok KuCancer Research Institute and Cancer Research Center, Seoul National University, Seoul 110-744, Korea.
Wook KimDepartment of Molecular Science and Technology, Ajou University, Suwon 443-749, Korea.
Sungjoo Kim YoonCancer Evolution Research Center, Catholic University of Korea, Seoul 137-701, Korea ; Department of Biomedical Science, College of Medicine, Catholic University of Korea, Seoul 137-701, Korea.
Hyo-Jeong KuhCancer Evolution Research Center, Catholic University of Korea, Seoul 137-701, Korea ; Department of Biomedical Science, College of Medicine, Catholic University of Korea, Seoul 137-701, Korea.
Jeong-Hwa LeeDepartment of Biochemistry, College of Medicine, Catholic University of Korea, Seoul 137-701, Korea ; Cancer Evolution Research Center, Catholic University of Korea, Seoul 137-701, Korea.
Suk Woo NamCancer Evolution Research Center, Catholic University of Korea, Seoul 137-701, Korea ; Department of Pathology, College of Medicine, Catholic University of Korea, Seoul 137-701, Korea.
Eun Kyung LeeDepartment of Biochemistry, College of Medicine, Catholic University of Korea, Seoul 137-701, Korea ; Cancer Evolution Research Center, Catholic University of Korea, Seoul 137-701, Korea.
Catholic University of Korea · KRAjou University · KRSeoul National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Several types of genetic and epigenetic regulation have been implicated in the development of drug resistance, one significant challenge for cancer therapy. Although changes in the expression of non-coding RNA are also responsible for drug resistance, the specific identities and roles of them remain to be elucidated. Long non-coding RNAs (lncRNAs) are a type of ncRNA (> 200 nt) that influence the regulation of gene expression in various ways. In this study, we aimed to identify differentially expressed lncRNAs in 5-fluorouracil-resistant colon cancer cells. Using two pairs of 5-FU-resistant cells derived from the human colon cancer cell lines SNU-C4 and SNU-C5, we analyzed the expression of 90 lncRNAs by qPCR-based profiling and found that 19 and 23 lncRNAs were differentially expressed in SNU-C4R and SNU-C5R cells, respectively. We confirmed that snaR and BACE1AS were downregulated in resistant cells. To further investigate the effects of snaR on cell growth, cell viability and cell cycle were analyzed after transfection of siRNAs targeting snaR. Down-regulation of snaR decreased cell death after 5-FU treatment, which indicates that snaR loss decreases in vitro sensitivity to 5-FU. Our results provide an important insight into the involvement of lncRNAs in 5-FU resistance in colon cancer cells.

Indexed as

Cell CycleCell DeathCell Growth ProcessesCell Line, TumorCell SurvivalColonic NeoplasmsDown-RegulationDrug Resistance, NeoplasmFluorouracilHumansRNA, Long NoncodingRNA, Small InterferingTranscriptomeBACE1-AS long non-coding RNA, humanFluorouracillong non-coding RNA snaR, humanRNA, Long NoncodingRNA, Small Interfering5-Fluorouracilcell viabilitydrug resistancelong non-coding RNAssnaR

Identifiers

PMID25078450
PMCPMC4132306
OpenAlexW1987715681

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.