Evidence map›Paper›PMID 32619088›Full record

ArticleCancer science2020

A nuclear lncRNA Linc00839 as a Myc target to promote breast cancer chemoresistance via PI3K/AKT signaling pathway.

Qi Chen, Huiling Shen, Xiaolan Zhu, Yueqin Liu, Hui Yang, Hui Chen, Shangwan Xiong, Huamao Chi, Wenlin Xu

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.6field-weighted citation impact, top 5% 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

37 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. EGR1/Cancer biology & therapy · 2023
    Article
  14. Review
  15. Review
  16. LOC101929709 promotes gastric cancer progression by aiding LIN28B to stabilize c-MYC mRNA.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2023
    Article
  17. Article
  18. Article
  19. Review
  20. Roles and Mechanisms of Long Non-Coding RNAs in Breast Cancer.International journal of molecular sciences · 2022
    Review
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

9 authors at 1 institution in 1 country.

Qi ChenDepartment of Breast Diseases, Fourth Affiliated Hospital of Jiangsu University, Zhenjiang, China.ORCID https://orcid.org/0000-0001-7070-4167
Huiling ShenDepartment of Oncology, Affiliated People Hospital of Jiangsu University, Zhenjiang, China.
Xiaolan ZhuCentral Laboratory, Fourth Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Yueqin LiuCentral Laboratory, Fourth Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Hui YangDepartment of Breast Diseases, Fourth Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Hui ChenSchool of medicine, Jiangsu University, Zhenjiang, China.
Shangwan XiongSchool of medicine, Jiangsu University, Zhenjiang, China.
Huamao ChiDepartment of Breast Diseases, Fourth Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Wenlin XuDepartment of Breast Diseases, Fourth Affiliated Hospital of Jiangsu University, Zhenjiang, China.ORCID https://orcid.org/0000-0001-7518-7912
Jiangsu University · CN

Funding

National Natural Science Foundation of China 81672913Social Development of Zhenjiang SH2017016Social Development Project of Jiangsu BE2018693
6 · The paper itself

Abstract

Chemoresistance has become a leading cause of mortality in breast cancer patients and is one of the major obstacles for improving the clinical outcome. Long noncoding RNAs play important roles in breast cancer tumorigenesis and chemoresistance. However, the involvement and regulation of lncRNAs in breast cancer chemoresistance are not completely understood. Here, we reported that Linc00839 was localized in the nucleus and upregulated in chemoresistant breast cancer cells and tissues, and high level of Linc00839 was associated with a poor prognosis. Knockdown of Linc00839 significantly suppressed proliferation, invasion, and migration, sensitized cells to paclitaxel in vitro and inhibited transplant tumor development in vivo. Mechanistically, we found that Myc could directly bind to the promoter region of Linc00839 and activate its transcription. Furthermore, Linc00839 overexpression increased the expression of Myc and the RNA-binding protein Lin28B and activated the PI3K/AKT signaling pathway. We also discovered that Lin28B positively interacted with Linc00839 and was upregulated in breast cancer tissues. Taken together, for the first time, we showed that Linc00839 was activated by Myc and promoted proliferation and chemoresistance in breast cancer through binding with Lin28B. These findings provide new insight into the regulatory mechanism of Linc00839 and propose a Myc/Linc00839/Lin28B feedback loop that could be used as a novel therapeutic target for breast cancer.

Indexed as

Genes, mycRNA InterferenceRNA, Long NoncodingAnimalsBreast NeoplasmsCell Line, TumorCell ProliferationDisease Models, AnimalDrug Resistance, NeoplasmFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansIn Situ Hybridization, FluorescenceMicePhosphatidylinositol 3-KinasesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA, Long Noncodingbreast cancerchemosensitivityLin28BLinc00839Myc

Identifiers

PMID32619088
PMCPMC7469761
OpenAlexW3039232790

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.