Evidence map›Paper›PMID 25955298›Full record

ArticleCell cycle (Georgetown, Tex.)2015

Let-7a regulates mammosphere formation capacity through Ras/NF-κB and Ras/MAPK/ERK pathway in breast cancer stem cells.

Chongwen Xu, Xin Sun, Sida Qin, Huangzhen Wang, Zhiwei Zheng, Shaohua Xu, Gang Luo, Peng Liu, Jian Liu, Ning Du and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2015. 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
2.9field-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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Lin28/let-7 axis in breast cancer.Molecular biology reports · 2025
    Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Unraveling the journey of cancer stem cells from origin to metastasis.Biochimica et biophysica acta. Reviews on cancer · 2019
    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

13 authors at 3 institutions in 1 country.

Chongwen Xua Second Department of Thoracic Surgery; First Affiliated Hospital; Medical College of Xi'an Jiaotong University ; Xi'an , Shaanxi ; PR China.
Xin Sun
Sida Qin
Huangzhen Wang
Zhiwei Zheng
Shaohua Xu
Gang Luo
Peng Liu
Jian Liu
Ning Du
Yunfeng Zhang
Dapeng Liu
Hong Ren
Xi'an Jiaotong University · CNPeople’s Hospital of Rizhao · CNShanghai First Maternity and Infant Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast cancer stem cells (BCSCs) have the greatest potential to maintain tumorigenesis in all subtypes of tumor cells and were regarded as the key drivers of tumor. Recent evidence has demonstrated that BCSCs contributed to a high degree of resistance to therapy. However, how BCSCs self renewal and tumorigenicity are maintained remains obscure. Herein, our study illustrated that overexpression of let-7a reduced cell proliferation and mammosphere formation ability of breast cancer stem cells(BCSCs) in a KRas-dependent manner through different pathways in vitro and in vivo. To be specific, we provided the evidence that let-7a was decreased, and reversely the expression of KRas was increased with moderate expression in early stages (I/II) and high expression in advanced stages (III/IV) in breast cancer specimens. In addition, the negative correlation between let-7a and KRas was clearly observed. In vitro, we found that let-7a inhibited mammosphere-forming efficiency and the mammosphere-size via NF-κB and MAPK/ERK pathway, respectively. The inhibitory effect of let-7a on mammosphere formation efficiency and the size of mammospheres was abolished after the depletion of KRas. On the contrary, enforced expression of KRas rescued the effect of let-7a. In vivo, let-7a inhibited the growth of tumors, whereas the negative effect of let-7a was rescued after overexpressing KRas. Taken together, our findings suggested that let-7a played a tumor suppressive role in a KRas-dependent manner.

Indexed as

Breast NeoplasmsDisease ProgressionFemaleHumansMAP Kinase Signaling SystemMicroRNAsNeoplastic Stem CellsNF-kappa BProto-Oncogene Proteins p21(ras)ras ProteinsSignal TransductionSpheroids, CellularTumor Suppressor ProteinsKRAS protein, humanMicroRNAsmirnlet7 microRNA, humanNF-kappa BProto-Oncogene Proteins p21(ras)ras ProteinsTumor Suppressor ProteinsBCSCs, breast cancer stem cellsbreast cancer stem cells, KRas, let-7amammosphere formation capacityMAPK/ERKMFE, mammosphere-forming efficiencyNF-κB

Identifiers

PMID25955298
PMCPMC4615052
OpenAlexW1604932993

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.