Evidence map›Paper›PMID 26909602›Full record

ArticleOncotarget2016

Role and mechanism of miR-222 in arsenic-transformed cells for inducing tumor growth.

Min Wang, Xin Ge, Jitai Zheng, Dongmei Li, Xue Liu, Lin Wang, Chengfei Jiang, Zhumei Shi, Lianju Qin, Jiayin Liu and 5 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

18 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Review
  3. miRNAs and arsenic-induced carcinogenesis.Advances in pharmacology (San Diego, Calif.) · 2023
    Review
  4. Review
  5. Review
  6. Review
  7. Paradoxical effects of arsenic in the lungs.Environmental health and preventive medicine · 2021
    Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. 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

15 authors at 4 institutions in 2 countries.

Min WangState Key Laboratory of Reproductive Medicine, Department of Pathology, and Collaborative Innovation Center for Cancer Personalized Medicine, Cancer Center, Nanjing Medical University, Nanjing, Jiangsu, China.
Xin GeState Key Laboratory of Reproductive Medicine, Department of Pathology, and Collaborative Innovation Center for Cancer Personalized Medicine, Cancer Center, Nanjing Medical University, Nanjing, Jiangsu, China.
Jitai ZhengState Key Laboratory of Reproductive Medicine, Department of Pathology, and Collaborative Innovation Center for Cancer Personalized Medicine, Cancer Center, Nanjing Medical University, Nanjing, Jiangsu, China.
Dongmei LiState Key Laboratory of Reproductive Medicine, Department of Pathology, and Collaborative Innovation Center for Cancer Personalized Medicine, Cancer Center, Nanjing Medical University, Nanjing, Jiangsu, China.
Xue LiuState Key Laboratory of Reproductive Medicine, Department of Pathology, and Collaborative Innovation Center for Cancer Personalized Medicine, Cancer Center, Nanjing Medical University, Nanjing, Jiangsu, China.
Lin WangState Key Laboratory of Reproductive Medicine, Department of Pathology, and Collaborative Innovation Center for Cancer Personalized Medicine, Cancer Center, Nanjing Medical University, Nanjing, Jiangsu, China.
Chengfei JiangState Key Laboratory of Reproductive Medicine, Department of Pathology, and Collaborative Innovation Center for Cancer Personalized Medicine, Cancer Center, Nanjing Medical University, Nanjing, Jiangsu, China.
Zhumei ShiState Key Laboratory of Reproductive Medicine, Department of Pathology, and Collaborative Innovation Center for Cancer Personalized Medicine, Cancer Center, Nanjing Medical University, Nanjing, Jiangsu, China.
Lianju QinCenter of Clinical Reproductive Medicine, Jiangsu Province Hospital, Nanjing, Jiangsu, China.
Jiayin LiuCenter of Clinical Reproductive Medicine, Jiangsu Province Hospital, Nanjing, Jiangsu, China.
Hushan YangDivision of Population Science, Department of Medical Oncology, Thomas Jefferson University, Philadelphia, PA, USA.
Ling-Zhi LiuDepartment of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, PA, USA.
Jun HeDepartment of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, PA, USA.
Linlin ZhenDepartment of Breast and Thyroid Surgery, Huai'an First People's Hospital, Huai'an, Jiangsu, China.
Bing-Hua JiangState Key Laboratory of Reproductive Medicine, Department of Pathology, and Collaborative Innovation Center for Cancer Personalized Medicine, Cancer Center, Nanjing Medical University, Nanjing, Jiangsu, China.
Nanjing Medical University · CNThomas Jefferson University · USJiangsu Province Hospital · CNHuaian First People’s Hospital · CN

Funding

Molecular Mechanism of Arsenic CarcinogenesisR01ES020868 · NIEHS · UNIVERSITY OF IOWA · PI JIANG, BINGHUA · 2014 to 2018
$1.7M
NOX4 Mediates Oxidative Stress in Ovarian Tumor growth and treatment ResponseR01CA193511 · NCI · UNIVERSITY OF IOWA · PI HE, JUN · 2016 to 2020
$1.7M
NCI NIH HHS R01 CA193511NCI NIH HHS R01CA193511NIEHS NIH HHS R01 ES020868NIEHS NIH HHS R01ES020868
6 · The paper itself

Abstract

High levels of arsenic in drinking water, soil, and air are associated with the higher incidences of several kinds of cancers worldwide, but the mechanism is yet to be fully discovered. Recently, a number of evidences show that dysregulation of microRNAs (miRNAs) induces carcinogenesis. In this study, we found miR-222 was upregulated in arsenic-transformed human lung epithelial BEAS-2B cells (As-T cells). Anti-miR-222 inhibitor treatment decreased cell proliferation, migration, tube formation, and induced apoptosis. In addition, anti-miR-222 inhibitor expression decreased tumor growth in vivo. We also found that inhibition of miR-222 induced the expression of its direct targets ARID1A and phosphatase and tensin homolog deleted on chromosome 10 (PTEN), and activated apoptosis of As-T cells in part through ARID1A downregulation. These results indicate that miR-222 plays an important role in arsenic-induced tumor growth.

Indexed as

AnimalsApoptosisArsenicArsenic PoisoningCell Line, TransformedCell Line, TumorCell ProliferationCell Transformation, NeoplasticHumansHuman Umbilical Vein Endothelial CellsLung NeoplasmsMiceMice, Inbred BALB CMice, NudeMicroRNAsPTEN PhosphohydrolaseArsenicMicroRNAsMIR222, humanPTEN PhosphohydrolasePTEN protein, humanARID1ABEAS-2B cellsmiR-222PTENtumor growth

Identifiers

PMID26909602
PMCPMC4951251
OpenAlexW2308535761

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.