Evidence map›Paper›PMID 33251678›Full record

ArticleCancer science2021

MiR-320b/RAD21 axis affects hepatocellular carcinoma radiosensitivity to ionizing radiation treatment through DNA damage repair signaling.

Jianyang Wang, Hong Zhao, Jing Yu, Xin Xu, Hao Jing, Ning Li, Yuan Tang, Shulian Wang, Yexiong Li, Jianqiang Cai and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

32 citing papers in PubMed, 42 citations in OpenAlex.

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  15. Comparative Transcriptomic Analysis of Three Common Liver Cell Lines.International journal of molecular sciences · 2023
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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

11 authors at 2 institutions in 1 country.

Jianyang WangDepartment of Radiation Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Hong ZhaoDepartment of Hepatobiliary Surgery, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Jing YuHubei Key Laboratory of Tumor Biological Behaviors, Zhongnan Hospital of Wuhan University, Wuhan, China.
Xin XuDepartment of Radiation Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Hao JingDepartment of Radiation Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Ning LiDepartment of Radiation Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Yuan TangDepartment of Radiation Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Shulian WangDepartment of Radiation Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Yexiong LiDepartment of Radiation Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Jianqiang CaiDepartment of Hepatobiliary Surgery, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Jing JinDepartment of Radiation Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.ORCID https://orcid.org/0000-0002-6645-5214
Chinese Academy of Medical Sciences & Peking Union Medical College · CNWuhan University · CN

Funding

Chinese Academy of Medical Sciences Innovation Fund 2017-I2M-1-005Chinese Academy of Medical Sciences Innovation Fund 2017-I2M-2-005National Key Research &Development Program of China 2016YFC0904600National Key Research &Development Program of China 2017YFC1311000National Natural Science Foundation of China 81602168National Natural Science Foundation of China 81773241
6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is one of the most common malignancies in the world and is associated with high mortality. Ionizing radiation (IR)-based therapy causes DNA damage, exerting a curative effect; however, DNA damage repair signaling pathways lead to HCC resistance to IR-based therapy. RAD21 is a component of the cohesion complex, crucial for chromosome segregation and DNA damage repair, while it is still unclear whether RAD21 is implicated in DNA damage and influences IR sensitivity in HCC. The current research explores the effect and upstream regulatory mechanism of RAD21 on IR sensitivity in HCC. In the present study, RAD21 mRNA and protein expression were increased within HCC tissue samples, particularly within IR-insensitive HCC tissues. The overexpression of RAD21 partially attenuated the roles of IR in HCC by promoting the viability and suppressing the apoptosis of HCC cells. RAD21 overexpression reduced the culture medium 8-hydroxy-2-deoxyguanosine concentration and decreased the protein levels of γH2AX and ATM, suggesting that RAD21 overexpression attenuated IR treatment-induced DNA damage to HCC cells. miR-320b targeted RAD21 3'-UTR to inhibit RAD21 expression. In HCC tissues, particularly in IR-insensitive HCC tissues, miR-320b expression was significantly downregulated. miR-320b inhibition also attenuated IR treatment-induced DNA damage to HCC cells; more importantly, RAD21 silencing significantly attenuated the effects of miR-320b inhibition on IR treatment-induced DNA damage, suggesting that miR-320b plays a role through targeting RAD21. In conclusion, an miR-320b/RAD21 axis modulating HCC sensitivity to IR treatment through acting on IR-induced DNA damage was demonstrated. The miR-320b/RAD21 axis could be a novel therapeutic target for further study of HCC sensitivity to IR treatment.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsAnimalsCell Cycle ProteinsDNA-Binding ProteinsDNA RepairGene Expression Regulation, NeoplasticHumansMiceMice, NudeMicroRNAsRadiation ToleranceRadiotherapySignal TransductionXenograft Model Antitumor AssaysCell Cycle ProteinsDNA-Binding ProteinsMicroRNAsMIRN320 microRNA, humanRAD21 protein, humanDNA damagehepatocellular carcinomaionizing radiation-based therapymiR-320bRAD21

Identifiers

PMID33251678
PMCPMC7894001
OpenAlexW3108592360

What OpenQuestion holds

Textmetadata
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.