Evidence map›Paper›PMID 31464090›Full record

ArticleCancer medicine2019

RIG-I promotes IFN/JAK2 expression and the endoplasmic reticulum stress response to inhibit chemoradiation resistance in nasopharyngeal carcinoma.

Di Jing, Weibing Zhou, Lin Shen, Qian Zhang, Wang-Ti Xie, Erdong Shen, Zhi Li, Liang-Fang Shen, Lun-Quan Sun

Open access · goldAbstract read
In one paragraph

Article in Cancer medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

16 citing papers in PubMed, 19 citations in OpenAlex.

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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.

Di JingDepartment of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Weibing ZhouDepartment of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Lin ShenDepartment of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Qian ZhangTeaching and Research Section of Surgery, Xiangnan University Affiliated Hospital, Chenzhou, Hunan, China.
Wang-Ti XieDepartment of Oncology, The First People's Hospital of YueYang, Yue Yang, Hunan, China.
Erdong ShenDepartment of Oncology, The First People's Hospital of YueYang, Yue Yang, Hunan, China.
Zhi LiCenter for Molecular Medicine, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Liang-Fang ShenDepartment of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan, China.ORCID 0000-0002-6429-7531
Lun-Quan SunCenter for Molecular Medicine, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Central South University · CNYueyang Second People's Hospital · CNXiangnan University · CN

Funding

Hunan Provincial Natural Science Foundation of China 2018JJ6123National Natural Science Foundation of China 81572612National Natural Science Foundation of China 81602406
6 · The paper itself

Abstract

RIG-I is associated with the occurrence and development of many tumors. However, the role of RIG-I in radiotherapy and chemotherapy in NPC has not been reported to date. In our study, RIG-I expression was significantly reduced in chemoradiotherapy-resistant NPC tissues and cells compared with that in therapy-sensitive tissues and cells. RIG-I expression increased in nonresistant NPC cells, including CNE1 and CNE2, in a dose-dependent manner with increasing chemotherapy drug concentration or radiotherapy dose. RIG-I overexpression promoted radiotherapy and chemotherapy sensitivity in NPC cells, leading to cellular apoptosis and increased expression of the proapoptotic factors BAX and caspase-3. Similarly, RIG-I knockdown in NPC cells promoted chemoradiotherapy resistance and reduced apoptosis. Analysis of microarray data indicated that the expression of IFN/JAK2 and endoplasmic reticulum (ER) stress response markers, such as JAK2, STAT1, IRF9, IFNB1, IRF3, p-IRF3, XBP1, ATF6, IFIT2, and ISG15, was inhibited in chemoradiotherapy-resistant cells compared with that in sensitive cells. Conversely, activation of IFN/JAK2 and ER stress response pathways in NPC cells reduced paclitaxel resistance and increased apoptosis. RIG-I promotes IFN/JAK2 and ER stress response-mediated apoptosis to inhibit chemoradiation resistance in nasopharyngeal carcinoma.

Indexed as

Drug Resistance, NeoplasmEndoplasmic Reticulum StressGene Expression Regulation, NeoplasticRadiation ToleranceAdultAgedAnimalsApoptosisCell Line, TumorCell SurvivalChemoradiotherapyDEAD Box Protein 58Disease Models, AnimalFemaleHeterograftsHumansDEAD Box Protein 58InterferonsJAK2 protein, humanJanus Kinase 2Receptors, ImmunologicRIGI protein, humanapoptosisendoplasmic reticulum stressIFN/JAK2radiotherapy and chemotherapy resistanceRIG-I

Identifiers

PMID31464090
PMCPMC6797570
OpenAlexW2971110256

What OpenQuestion holds

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LicenceCC BY
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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.