Evidence map›Paper›PMID 31201367›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2019

miR-26a promotes hepatocellular carcinoma invasion and metastasis by inhibiting PTEN and inhibits cell growth by repressing EZH2.

Wen-Tao Zhao, Xiao-Lin Lin, Yu Liu, Liu-Xin Han, Jing Li, Tao-Yan Lin, Jun-Wen Shi, Sheng-Chun Wang, Mei Lian, Heng-Wei Chen and 5 more

Abstract read
PubMed Publisher
In one paragraph

Article in Laboratory investigation; a journal of technical methods and pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

  1. Pooled it
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  15. MicroRNAs Regulate Cell Cycle and Cell Death Pathways in Glioblastoma.International journal of molecular sciences · 2021
    Review
  16. Article
  17. Article
  18. mAging · 2021
    Article
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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

15 authors at 5 institutions in 1 country.

Wen-Tao ZhaoGuangdong Provincial Key Laboratory of Cancer Immunotherapy Research and Guangzhou Key Laboratory of Tumor Immunology Research, Cancer Research Institute, School of Basic Medical Science, Southern Medical University, Guangzhou, 510515, China.
Xiao-Lin LinGuangdong Provincial Key Laboratory of Cancer Immunotherapy Research and Guangzhou Key Laboratory of Tumor Immunology Research, Cancer Research Institute, School of Basic Medical Science, Southern Medical University, Guangzhou, 510515, China.
Yu LiuInstitute of Comparative Medicine & Laboratory Animal Center, Southern Medical University, Guangzhou, 510515, China.
Liu-Xin HanThe Third People's Hospital of Kunming, Kunming, 650041, China.
Jing LiGuangdong Provincial Key Laboratory of Cancer Immunotherapy Research and Guangzhou Key Laboratory of Tumor Immunology Research, Cancer Research Institute, School of Basic Medical Science, Southern Medical University, Guangzhou, 510515, China.
Tao-Yan LinGuangdong Provincial Key Laboratory of Cancer Immunotherapy Research and Guangzhou Key Laboratory of Tumor Immunology Research, Cancer Research Institute, School of Basic Medical Science, Southern Medical University, Guangzhou, 510515, China.
Jun-Wen ShiGuangdong Provincial Key Laboratory of Cancer Immunotherapy Research and Guangzhou Key Laboratory of Tumor Immunology Research, Cancer Research Institute, School of Basic Medical Science, Southern Medical University, Guangzhou, 510515, China.
Sheng-Chun WangGuangdong Provincial Key Laboratory of Cancer Immunotherapy Research and Guangzhou Key Laboratory of Tumor Immunology Research, Cancer Research Institute, School of Basic Medical Science, Southern Medical University, Guangzhou, 510515, China.
Mei LianInstitute of Comparative Medicine & Laboratory Animal Center, Southern Medical University, Guangzhou, 510515, China.
Heng-Wei ChenInstitute of Comparative Medicine & Laboratory Animal Center, Southern Medical University, Guangzhou, 510515, China.
Yan SunZhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, China.
Kang XuDepartment of General Surgery, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
Jun-Shuang JiaGuangdong Provincial Key Laboratory of Cancer Immunotherapy Research and Guangzhou Key Laboratory of Tumor Immunology Research, Cancer Research Institute, School of Basic Medical Science, Southern Medical University, Guangzhou, 510515, China. Jiajsh4@126.com.
Rong-Cheng LuoCancer Center, Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, Guangzhou, Guangdong, 510315, China. luorc01@163.com.
Dong XiaoGuangdong Provincial Key Laboratory of Cancer Immunotherapy Research and Guangzhou Key Laboratory of Tumor Immunology Research, Cancer Research Institute, School of Basic Medical Science, Southern Medical University, Guangzhou, 510515, China. Xiao_d@hotmail.com.
Southern Medical University · CNKunming Third People's Hospital · CNSun Yat-sen Memorial Hospital · CNSun Yat-sen University · CNTCM-Intigrated Cancer Center of Southern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A previous study revealed that therapeutic miR-26a delivery suppresses tumorigenesis in a murine liver cancer model, whereas we found that forced miR-26a expression increased hepatocellular carcinoma (HCC) cell migration and invasion, which prompted us to characterize the causes and mechanisms underlying enhanced invasion due to ectopic miR-26a expression. Gain-of-function and loss-of-function experiments demonstrated that miR-26a promoted migration and invasion of BEL-7402 and HepG2 cells in vitro and positively modulated matrix metalloproteinase (MMP)-1, MMP-2, MMP-9, and MMP-10 expression. In addition, exogenous miR-26a expression significantly enhanced the metastatic ability of HepG2 cells in vivo. miR-26a negatively regulated in vitro proliferation of HCC cells, and miR-26a overexpression suppressed HepG2 cell tumor growth in nude mice. Further studies revealed that miR-26a inhibited cell growth by repressing the methyltransferase EZH2 and promoted cell migration and invasion by inhibiting the phosphatase PTEN. Furthermore, PTEN expression negatively correlated with miR-26a expression in HCC specimens from patients with and without metastasis. Thus, our findings suggest for the first time that miR-26a promotes invasion/metastasis by inhibiting PTEN and inhibits cell proliferation by repressing EZH2 in HCC. More importantly, our data also suggest caution if miR-26a is used as a target for cancer therapy in the future.

Indexed as

AnimalsCarcinoma, HepatocellularCell MovementEnhancer of Zeste Homolog 2 ProteinFemaleHep G2 CellsHumansLiver NeoplasmsMice, Inbred BALB CMice, NudeMicroRNAsNeoplasm MetastasisPTEN PhosphohydrolaseEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanMicroRNAsMIRN26 microRNA, humanPTEN PhosphohydrolasePTEN protein, human

Identifiers

PMID31201367
OpenAlexW2953108711

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.