↓ Skip to main content

RETRACTED ARTICLE: Long noncoding RNA MLK7-AS1 promotes ovarian cancer cells progression by modulating miR-375/YAP1 axis

Overview of attention for article published in Journal of Experimental & Clinical Cancer Research, September 2018
Altmetric Badge

About this Attention Score

  • Good Attention Score compared to outputs of the same age (69th percentile)
  • High Attention Score compared to outputs of the same age and source (84th percentile)

Mentioned by

twitter
6 X users
googleplus
1 Google+ user

Citations

dimensions_citation
66 Dimensions

Readers on

mendeley
14 Mendeley
You are seeing a free-to-access but limited selection of the activity Altmetric has collected about this research output. Click here to find out more.
Title
RETRACTED ARTICLE: Long noncoding RNA MLK7-AS1 promotes ovarian cancer cells progression by modulating miR-375/YAP1 axis
Published in
Journal of Experimental & Clinical Cancer Research, September 2018
DOI 10.1186/s13046-018-0910-4
Pubmed ID
Authors

Huan Yan, Hong Li, Pengyun Li, Xia Li, Jianjian Lin, Linlin Zhu, Maria A. Silva, Xiaofang Wang, Ping Wang, Zhan Zhang

Abstract

Long noncoding RNAs (LncRNAs) have been reported to be abnormally expressed in human ovarian cancer and associated with the proliferation and metastasis of cancer cells. The objective of this study was to investigate the role and the underlying mechanisms of LncRNA MAP3K20 antisense RNA 1 (MLK7-AS1) in ovarian cancer. The expression level of MLK7-AS1 was investigated in human ovarian cancer tissues and cell lines. The effects of MLK7-AS1 knockdown on ovarian cancer cell proliferation, migration, invasion and apoptosis were evaluated in vitro using MTT, colony formation assays, wound healing assays, transwell assays and flow cytometry. Furthermore, the in vivo effects were determined using the immunodeficient NSG female mice. Luciferase reporter assays were employed to identify interactions among MLK7-AS1 and its target genes. In the current study, MLK7-AS1 was specifically upregulated in ovarian cancer tissues and cell lines. Knockdown of MLK7-AS1 inhibited the ability of cell migration, invasion, proliferation, colony formation and wound healing, whereas promoted cell apoptosis in vitro. By using online tools and mechanistic analysis, we demonstrated that MLK7-AS1 could directly bind to miR-375 and downregulate its expression. Besides, MLK7-AS1 reversed the inhibitory effect of miR-375 on the growth of ovarian cancer cells, which might be involved in the upregulation of Yes-associated protein 1 (YAP1) expression. Moreover, knockdown MLK7-AS1 expression inhibited primary tumor growth in ovary and metastatic tumors in multiple peritoneal organs including liver and spleen in vivo, which were partly abolished by miR-375 inhibition. Mechanically, we found that MLK7-AS1 modulated the epithelial-mesenchymal transition (EMT) process by interacting with miR-375/YAP1 both in vivo and vitro, which promoted the expression of Slug. Taken together, our study showed for the first time that MLK7-AS1 interacted with miR-375 to promote proliferation, metastasis, and EMT process in ovarian cancer cells through upregulating YAP1.

X Demographics

X Demographics

The data shown below were collected from the profiles of 6 X users who shared this research output. Click here to find out more about how the information was compiled.
Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 14 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 14 100%

Demographic breakdown

Readers by professional status Count As %
Other 2 14%
Student > Ph. D. Student 2 14%
Lecturer > Senior Lecturer 1 7%
Lecturer 1 7%
Student > Bachelor 1 7%
Other 3 21%
Unknown 4 29%
Readers by discipline Count As %
Medicine and Dentistry 3 21%
Nursing and Health Professions 2 14%
Agricultural and Biological Sciences 1 7%
Biochemistry, Genetics and Molecular Biology 1 7%
Immunology and Microbiology 1 7%
Other 1 7%
Unknown 5 36%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 6. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 04 October 2021.
All research outputs
#6,484,414
of 25,385,509 outputs
Outputs from Journal of Experimental & Clinical Cancer Research
#365
of 2,382 outputs
Outputs of similar age
#106,615
of 350,625 outputs
Outputs of similar age from Journal of Experimental & Clinical Cancer Research
#11
of 69 outputs
Altmetric has tracked 25,385,509 research outputs across all sources so far. This one has received more attention than most of these and is in the 74th percentile.
So far Altmetric has tracked 2,382 research outputs from this source. They receive a mean Attention Score of 4.8. This one has done well, scoring higher than 84% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 350,625 tracked outputs that were published within six weeks on either side of this one in any source. This one has gotten more attention than average, scoring higher than 69% of its contemporaries.
We're also able to compare this research output to 69 others from the same source and published within six weeks on either side of this one. This one has done well, scoring higher than 84% of its contemporaries.