Evidence map›Paper›PMID 28270206›Full record

ArticleBMC cancer2017

MEIS1 inhibits clear cell renal cell carcinoma cells proliferation and in vitro invasion or migration.

Jie Zhu, Liang Cui, Axiang Xu, Xiaotao Yin, Fanglong Li, Jiangping Gao

Abstract read
In one paragraph

Article in BMC cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
–field-weighted citation impact
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

27 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. MEIS1-mediated Apoptosis via TNFR1 in Endometriosis.Reproductive sciences (Thousand Oaks, Calif.) · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. SALL4 Oncogenic Function in Cancers: Mechanisms and Therapeutic Relevance.International journal of molecular sciences · 2022
    Review
  13. Review
  14. Article
  15. MEIS1 and its potential as a cancer therapeutic target (Review).International journal of molecular medicine · 2021
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Oncogenic and tumor suppressor function of MEIS and associated factors.Turkish journal of biology = Turk biyoloji dergisi · 2020
    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

6 authors.

Jie ZhuDepartment of Urology, Chinese PLA Medical School/Chinese PLA General Hospital, Beijing, 100853, People's Republic of China.
Liang CuiDepartment of Urology, Chinese PLA Medical School/Chinese PLA General Hospital, Beijing, 100853, People's Republic of China.
Axiang XuDepartment of Urology, Chinese PLA Medical School/Chinese PLA General Hospital, Beijing, 100853, People's Republic of China.
Xiaotao YinDepartment of Urology, Chinese PLA Medical School/Chinese PLA General Hospital, Beijing, 100853, People's Republic of China.
Fanglong LiDepartment of Urology, Chinese PLA Medical School/Chinese PLA General Hospital, Beijing, 100853, People's Republic of China.
Jiangping GaoDepartment of Urology, Chinese PLA Medical School/Chinese PLA General Hospital, Beijing, 100853, People's Republic of China. jpgao@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMyeloid ecotropic viral integration site 1 (MEIS1) protein plays a synergistic causative role in acute myeloid leukemia (AML). However, MEIS1 has also shown to be a potential tumor suppressor in some other cancers, such as non-small-cell lung cancer (NSCLC) and prostate cancer. Although multiple roles of MEIS1 in cancer development and progression have been identified, there is an urgent demand to discover more functions of this molecule for further therapeutic design.

methodsMEIS1 was overexpressed via adenovirus vector in clear cell renal cell carcinoma (ccRCC) cells. Western blot and real-time qPCR (quantitative Polymerase Chain Reaction) was performed to examine the protein and mRNA levels of MEIS1. Cell proliferation, survival, in vitro migration and invasion were tested by MTT, colony formation, soft-agar, transwell (in vitro invasion/migration) assays, and tumor in vivo growthwas measured on nude mice model. In addition, flow-cytometry analysis was used to detect cell cycle arrest or non-apoptotic cell death of ccRCC cells induced by MEIS1.

resultsMEIS1 exhibits a decreased expression in ccRCC cell lines than that in non-tumor cell lines. MEIS1 overexpression inhibits ccRCC cells proliferation and induces G1/S arrest concomitant with marked reduction of G1/S transition regulators, Cyclin D1 and Cyclin A. Moreover, MEIS1-1 overexpression also induces non-apoptotic cell death of ccRCC cells via decreasing the levels of pro-survival regulators Survivin and BCL-2. Transwell migration assay (TMA) shows that MEIS1 attenuates in vitro invasion and migration of ccRCC cells with down-regulated epithelial-mesenchymal transition (EMT) process. Further, in nude mice model, MEIS1 inhibits the in vivo growth of Caki-1 cells.

conclusionsBy investigating the role of MEIS1 in ccRCC cells' survival, proliferation, anchorage-independent growth, cell cycle progress, apoptosis and metastasis, in the present work, we propose that MEIS1 may play an important role in clear cell renal cell carcinoma (ccRCC) development.

Indexed as

AnimalsApoptosisCarcinoma, Renal CellCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansInhibitor of Apoptosis ProteinsMiceMyeloid Ecotropic Viral Integration Site 1 ProteinNeoplasm InvasivenessProto-Oncogene Proteins c-bcl-2Signal TransductionSurvivinBIRC5 protein, humanInhibitor of Apoptosis ProteinsMEIS1 protein, humanMyeloid Ecotropic Viral Integration Site 1 ProteinProto-Oncogene Proteins c-bcl-2SurvivinClear cell renal cell carcinomain vitro invasion or migrationMEIS1Proliferation

Identifiers

PMID28270206
PMCPMC5341457

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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.