Evidence map›Paper›PMID 31034464›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2019

Improved Radiotherapy Sensitivity of Nasopharyngeal Carcinoma Cells by miR-29-3p Targeting COL1A1 3'-UTR.

Ying Guo, Jianhua Zhai, Jing Zhang, Changbao Ni, Huifang Zhou

Open access · hybridAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

20 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. Review
  3. Astaxanthin suppresses the malignant behaviors of nasopharyngeal carcinoma cells by blocking PI3K/AKT and NF-κB pathways via miR-29a-3p.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2024
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  13. MicroRNA-29b regulates the radiosensitivity of esophageal squamous cell carcinoma by regulating the BTG2-mediated cell cycle.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2021
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  20. Observational
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.

Ying GuoDepartment of Otorhinolaryngology, Tianjin Medical University General Hospital, Tianjin, China (mainland).
Jianhua ZhaiDepartment of Emergency Medicine, Tianjin Medical University General Hospital, Tianjin, China (mainland).
Jing ZhangDepartment of Otorhinolaryngology, Tianjin Medical University General Hospital, Tianjin, China (mainland).
Changbao NiDepartment of Otorhinolaryngology, Tianjin Medical University General Hospital, Tianjin, China (mainland).
Huifang ZhouDepartment of Otorhinolaryngology, Tianjin Medical University General Hospital, Tianjin, China (mainland).
Tianjin Medical University General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND Radio-resistance is an obstacle to the treatment of human nasopharyngeal carcinoma (NPC). However, how microRNAs (miRNA) are involved in this process remains unclear. In the present study we explored the role and possible molecular mechanism of miR-29a-3p, formerly known as tumor suppressors, in radio-sensitivity of NPC cells. MATERIAL AND METHODS A radio-resistant sub-cell line, CNE-2R, was established to detect the expression of miR-29a/b/c-3p using qRT-PCR. CCK-8 assay, colony formation assay, and single-cell gel electrophoresis (SCGE) assay were carried out to analyze the radio-sensitivity of NPC cells. qRT-PCR, luciferase reporter, and Western blot experiments were performed to validate the targeting of COL1A1 by miR-29a. Short interference RNAs (siRNAs) were used to investigate whether COL1A1 mediates the radio-sensitizer role of miR-29a. Expression of miR-29a and COL1A1 in radio-resistant NPC tissues was finally determined. RESULTS miR-29a was decreased in the radio-resistant CNE-2R cells. Following a time-course irradiation (IR) exposure, miR-29a exhibited a time-dependent decrease. Cellular experiments confirmed that miR-29a induced radio-sensitivity of CNE-2R cells via suppressing cell viability and enhancing cell apoptosis after IR. We confirmed that COL1A1 is a direct target of miR-29a and can exert radio-resistance effects in NPC cells. We also found that knockdown of COL1A1 inhibits NPC cell viability and sensitivity to IR. Finally, we observed a downregulation of miR-29a in radio-resistant NPC tissues and its decrease was associated with upregulation of COL1A1. CONCLUSIONS miR-29a is a critical determinant of NPC radio-response for NPC patients, and its induction provides a promising therapeutic choice to elevate NPC radio-sensitivity.

Indexed as

3' Untranslated RegionsApoptosisCell Line, TumorCell ProliferationCell SurvivalCollagen Type ICollagen Type I, alpha 1 ChainGene Knockdown TechniquesHumansMicroRNAsNasopharyngeal CarcinomaNasopharyngeal NeoplasmsRadiation ToleranceTransfectionUp-Regulation3' Untranslated RegionsCollagen Type ICollagen Type I, alpha 1 ChainMicroRNAsMIRN29a microRNA, human

Identifiers

PMID31034464
PMCPMC6503752
OpenAlexW2942621689

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.