Evidence map›Paper›PMID 32965597›Full record

ArticleMolecular and cellular biochemistry2021

LncRNA MALAT1 mediates doxorubicin resistance of hepatocellular carcinoma by regulating miR-3129-5p/Nova1 axis.

Yongxian Cao, Feng Zhang, Haotian Wang, Chunhua Bi, Jinpeng Cui, Fenghai Liu, Huazheng Pan

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular and cellular biochemistry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.8field-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

28 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Article
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  4. Review
  5. Hepatocellular carcinoma drug resistance models.Cancer cell international · 2025
    Review
  6. Review
  7. Review
  8. N6-methyladenosine-modified long non-coding RNAWorld journal of gastroenterology · 2024
    Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. miRNAs as short non-coding RNAs in regulating doxorubicin resistance.Journal of cell communication and signaling · 2023
    Review
  17. Article
  18. Review
  19. Article
  20. Article
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

7 authors at 4 institutions in 1 country.

Yongxian Cao *Department of Clinical Laboratory, The Affiliated Hospital of Qingdao University, No. 16, Jiangsu Road, Qingdao, 266003, Shandong, China.
Feng Zhang *Department of Clinical Laboratory, Rizhao City Hospital of Traditional Chinese Medicine, Rizhao, Shandong, China.
Haotian WangMedical College, Yanbian University, Yanji, Jilin, China.
Chunhua BiDepartment of Infectious Disease, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China.
Jinpeng CuiDepartment of Clinical Laboratory, Yantaishan Hospital, Yantai, Shandong, China.
Fenghai LiuDepartment of Clinical Laboratory, Qingdao Municipal Hospital, No. 5, Middle Donghai Road, Qingdao, 266071, Shandong, China. qvnyls@163.com.
Huazheng PanDepartment of Clinical Laboratory, The Affiliated Hospital of Qingdao University, No. 16, Jiangsu Road, Qingdao, 266003, Shandong, China. panhuazheng2019@163.com.ORCID http://orcid.org/0000-0001-9877-9881
Qingdao University · CNPeople’s Hospital of Rizhao · CNYanbian University · CNYantaishan Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Drug resistance is one of the major challenges for cancer therapies. In recent years, research on disease-related molecular signaling pathways has become the key ways to understand and overcome obstacles. Dysregulation of MALAT1 could regulate doxorubicin resistance of hepatocellular carcinoma (HCC), but how MALAT1 involving in managing doxorubicin resistance remains unclear yet. We aimed to elucidate the specific molecular mechanism of MALAT1 with doxorubicin resistance in HCC cells. Quantitative real-time polymerase chain reaction (qRT-PCR) was engaged to detect the expression levels of MALAT1, miR-3129-5p and Nova1 mRNA; MTT, western blot, flow cytometry and luciferase reporter assays were executed to identify the influence of MALAT1 on doxorubicin resistance of HCC cells. Xenograft tumor model was created to confirm the biological function of MALAT1 in doxorubicin resistance of HCC cells in vivo. MALAT1 and Nova1 were upregulated, while miR-3129-5p expression was decreased in doxorubicin-resistant HCC tissues and cells. Knockdown of MALAT1 regulated doxorubicin resistance of HCC cells through inhibiting cell proliferation, migration, invasion and promoting apoptosis, but antisense miR-3129-5p released the functional effect of MALAT1 knockdown. Nova1, as a target gene of miR-3129-5p, reversed the results of miR-3129-5p expression and enhanced doxorubicin resistance of HCC cells. Xenograft tumor model suggested that dysregulation of MALAT1 regulated tumor growth and Nova1 to mediate doxorubicin resistance of HCC cells by as a sponge for miR-3129-5p in vivo. Elevation of LncRNA MALAT1 mediated doxorubicin resistance and the progression of HCC via a MALAT1/miR-3129-5p/Nova1 axis. This study would be expected to enrich the understanding of doxorubicin resistance of HCC and provide new ideas for HCC treatment strategies.

Indexed as

AnimalsApoptosisCarcinoma, HepatocellularCell Line, TumorCell MovementCell ProliferationDoxorubicinDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHumansLiver NeoplasmsMiceMice, NudeMicroRNAsNeoplasm InvasivenessNeoplasm TransplantationDoxorubicinMALAT1 long non-coding RNA, humanMalat1 long non-coding RNA, mouseMicroRNAsMIRN3129 microRNA, humanNeuro-Oncological Ventral AntigenNOVA1 protein, humanNova1 protein, mouseRNA-Binding ProteinsRNA, Long NoncodingChemotherapyDoxorubicin resistanceHCCMALAT1miR-3129-5pNova1

Identifiers

PMID32965597
OpenAlexW3088389433

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.