Evidence map›Paper›PMID 19726678›Full record

ArticleThe Journal of biological chemistry2009

MicroRNA-122 inhibits tumorigenic properties of hepatocellular carcinoma cells and sensitizes these cells to sorafenib.

Shoumei Bai, Mohd W Nasser, Bo Wang, Shu-Hao Hsu, Jharna Datta, Huban Kutay, Arti Yadav, Gerard Nuovo, Pawan Kumar, Kalpana Ghoshal

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 266 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
266citing papers in PubMed, 4 pooled it
13.4field-weighted citation impact, top 1% 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

266 citing papers in PubMed, 4 syntheses or guidelines pooled it, 477 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Trial
  6. International journal of molecular sciences · 2026
    Article
  7. Review
  8. Article
  9. Non-coding RNAs in alcohol-associated liver disease.Liver research (Beijing, China) · 2025
    Review
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  18. The Impact of miR-122 on Cancer.Current pharmaceutical biotechnology · 2024
    Review
  19. Review
  20. Article

206 more citing papers are in PubMed but not listed here.

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

10 authors at 1 institution in 1 country.

Shoumei BaiDepartment of Molecular and Cellular Biochemistry, The Ohio State University, Columbus, Ohio 43210, USA.
Mohd W Nasser
Bo Wang
Shu-Hao Hsu
Jharna Datta
Huban Kutay
Arti Yadav
Gerard Nuovo
Pawan Kumar
Kalpana Ghoshal
The Ohio State University · US

Funding

MOLECULAR MECHANISMS OF DIET-INDUCED CARCINOGENESISR01CA086978 · NCI · OHIO STATE UNIVERSITY · PI GHOSHAL, KALPANA, JACOB, SAMSON T · 2002 to 2018
$4.9M
The Role of MicroRNA in HepatocarcinogenesisR21CA122694 · NCI · OHIO STATE UNIVERSITY · PI GHOSHAL, KALPANA · 2006 to 2007
$309k
NCI NIH HHS CA086978NCI NIH HHS CA122694NCI NIH HHS R01 CA086978NCI NIH HHS R21 CA122694
6 · The paper itself

Abstract

MicroRNAs are negative regulators of protein coding genes. The liver-specific microRNA-122 (miR-122) is frequently suppressed in primary hepatocellular carcinomas (HCCs). In situ hybridization demonstrated that miR-122 is abundantly expressed in hepatocytes but barely detectable in primary human HCCs. Ectopic expression of miR-122 in nonexpressing HepG2, Hep3B, and SK-Hep-1 cells reversed their tumorigenic properties such as growth, replication potential, clonogenic survival, anchorage-independent growth, migration, invasion, and tumor formation in nude mice. Further, miR-122-expressing HCC cells retained an epithelial phenotype that correlated with reduced Vimentin expression. ADAM10 (a distintegrin and metalloprotease family 10), serum response factor (SRF), and insulin-like growth factor 1 receptor (Igf1R) that promote tumorigenesis were validated as targets of miR-122 and were repressed by the microRNA. Conversely, depletion of the endogenous miR-122 in Huh-7 cells facilitated their tumorigenic properties with concomitant up-regulation of these targets. Expression of SRF or Igf1R partially reversed tumor suppressor function of miR-122. Further, miR-122 impeded angiogenic properties of endothelial cells in vitro. Notably, ADAM10, SRF, and Igf1R were up-regulated in primary human HCCs compared with the matching liver tissue. Co-labeling studies demonstrated exclusive localization of miR-122 in the benign livers, whereas SRF predominantly expressed in HCC. More importantly, growth and clonogenic survival of miR-122-expressing HCC cells were significantly reduced upon treatment with sorafenib, a multi-kinase inhibitor clinically effective against HCC. Collectively, these results suggest that the loss of multifunctional miR-122 contributes to the malignant phenotype of HCC cells, and miR-122 mimetic alone or in combination with anticancer drugs can be a promising therapeutic regimen against liver cancer.

Indexed as

AnimalsAntineoplastic AgentsBenzenesulfonatesBlotting, WesternCarcinoma, HepatocellularCell ProliferationHumansIn Situ HybridizationLiver NeoplasmsLuciferasesMiceMice, NudeMicroRNAsNiacinamidePhenylurea CompoundsPyridinesAntineoplastic AgentsBenzenesulfonatesLuciferasesMicroRNAsMIRN122 microRNA, humanNiacinamidePhenylurea CompoundsPyridinesRNA, MessengerSorafenib

Identifiers

PMID19726678
PMCPMC2797273
OpenAlexW2073391234

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.