Evidence map›Paper›PMID 28291769›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2017

Downregulation of miR-33a-5p in Hepatocellular Carcinoma: A Possible Mechanism for Chemotherapy Resistance.

Wei Meng, Yan Tai, Hui Zhao, Binsheng Fu, Tong Zhang, Wei Liu, Hua Li, Yang Yang, Qi Zhang, Yuliang Feng and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2017. 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
2.7field-weighted citation impact, top 10% 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, 44 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

11 authors at 4 institutions in 2 countries.

Wei MengDepartment of Hepatic Surgery and Liver Transplantation Center of The Third Affiliated Hospital, Organ Transplantation Institute, Sun Yat-sen University; Organ Transplantation Research Center of Guangdong Province, Guangzhou, Guangdong, China (mainland).
Yan TaiGuangdong Key Laboratory of Liver Disease Research, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China (mainland).
Hui ZhaoDepartment of Hepatic Surgery and Liver transplantation Center of The Third Affiliated Hospital, Organ Transplantation Institute, Sun Yat-sen University; Organ Transplantation Research Center of Guangdong Province, Guangzhou, Guangdong, China (mainland).
Binsheng FuDepartment of Hepatic Surgery and Liver transplantation Center of The Third Affiliated Hospital, Organ Transplantation Institute, Sun Yat-sen University; Organ Transplantation Research Center of Guangdong Province, Guangzhou, Guangdong, China (mainland).
Tong ZhangDepartment of Hepatic Surgery and Liver transplantation Center of The Third Affiliated Hospital, Organ Transplantation Institute, Sun Yat-sen University; Organ Transplantation Research Center of Guangdong Province, Guangzhou, Guangdong, China (mainland).
Wei LiuGuangdong Key Laboratory of Liver Disease Research, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China (mainland).
Hua LiDepartment of Hepatic Surgery and Liver transplantation Center of The Third Affiliated Hospital, Organ Transplantation Institute, Sun Yat-sen University; Organ Transplantation Research Center of Guangdong Province, Guangzhou, Guangdong, China (mainland).
Yang YangDepartment of Hepatic Surgery and Liver transplantation Center of The Third Affiliated Hospital, Organ Transplantation Institute, Sun Yat-sen University; Organ Transplantation Research Center of Guangdong Province, Guangzhou, Guangdong, China (mainland).
Qi ZhangGuangdong Key Laboratory of Liver Disease Research, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China (mainland).
Yuliang FengJackson Laboratory-Genomic Medicine, Farmington, CT, USA.
Guihua ChenDepartment of Hepatic Surgery and Liver transplantation Center of The Third Affiliated Hospital, Organ Transplantation Institute, Sun Yat-sen University; Organ Transplantation Research Center of Guangdong Province, Guangzhou, Guangdong, China (mainland).
Sun Yat-sen University · CNKey Laboratory of Guangdong Province · CNThird Affiliated Hospital of Sun Yat-sen University · CNJackson Laboratory · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND Multi-drug resistance is one of the major problems limiting the efficacy of cisplatin (CDDP) in treatment of hepatocellular carcinoma (HCC), and abnormal microRNA (miRNA) expression in drug-resistant cell lines plays an important role in liver cancer chemotherapy resistance. MATERIAL AND METHODS We established stable Hep3B and 97L HCC cell strains resistant to CDDP, both in vitro and in vivo. A combination of microRNA microarray and RT-qPCR experiments were used to screen differentially expressed miRNAs in HCC cell strains. A CCK-8 assay was carried out to detect and calculate the survival rates and relative inhibitory rates. Oligonucleotide transfection was used to confirm the regulatory function of the miRNA in HCC drug resistance. RESULTS The IC50 of Hep3B/CDDP(v), 97L/CDDP(v), Hep3B/CDDP(s), and 97L/CDDP(s) were significantly higher than that of their parental cells. Moreover, the doubling time of drug-resistant cells increased compared with their parent cells. MiRCURYTM LNA Array (v 16.0) high-throughput tests of resistant cell models and their parent cells showed that there were 5 downregulated microRNAs in the 4 drug-resistant cell lines, and we chose hsa-miR-33a-5p as our target for further study. Oligonucleotide transfection showed that miR-33a-5p overexpression increased the cisplatin sensitivity of Hep3B/CDDP(v) and 97L/CDDP(v) drug-resistant cells and reduced their resistance. Additionally, inhibition of miR-33a-5p expression reduced cisplatin sensitivity in Hep3B and 97L and increased their drug resistance. CONCLUSIONS This study confirmed that the most downregulated microRNA, miR-33a-5p, can mediate the cisplatin resistance of HCC cells, providing a new and feasible direction for research into combatting liver cancer chemotherapy resistance.

Indexed as

AnimalsAntineoplastic AgentsCarcinoma, HepatocellularCell Line, TumorCisplatinDrug Resistance, MultipleDrug Resistance, NeoplasmDrug Screening Assays, AntitumorGene Expression Regulation, NeoplasticHumansLiver NeoplasmsMaleMiceMice, NudeMicroRNAsSignal TransductionAntineoplastic AgentsCisplatinMicroRNAsMIRN33a microRNA, human

Identifiers

PMID28291769
PMCPMC5362191
OpenAlexW2599027269

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.