Evidence map›Paper›PMID 30030896›Full record

ArticleCancer medicine2018

Long noncoding RNA LINC00152 promotes cell proliferation through competitively binding endogenous miR-125b with MCL-1 by regulating mitochondrial apoptosis pathways in ovarian cancer.

Puxiang Chen, Xiaolin Fang, Bing Xia, Yan Zhao, Qiaoyan Li, Xiaoying Wu

Abstract read
In one paragraph

Article in Cancer medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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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

40 citing papers in PubMed.

  1. Review
  2. Review
  3. Mechanisms of apoptosis-related non-coding RNAs in ovarian cancer: a narrative review.Apoptosis : an international journal on programmed cell death · 2025
    Review
  4. Review
  5. The Role of Long Non-Coding RNAs in Ovarian Cancer Cells.International journal of molecular sciences · 2024
    Review
  6. Review
  7. Review
  8. Article
  9. Cells · 2022
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Ovarian Cancer Stem Cells: Characterization and Role in Tumorigenesis.Advances in experimental medicine and biology · 2021
    Article
  17. Review
  18. Mechanisms of Apoptosis-Related Long Non-coding RNAs in Ovarian Cancer.Frontiers in cell and developmental biology · 2021
    Review
  19. Review
  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

6 authors.

Puxiang ChenDepartment of Gynecology and Obstetrics, The Second Xiangya Hospital of Central South University, Changsha, China.ORCID 0000-0003-2600-0490
Xiaolin FangDepartment of Gynecology and Obstetrics, The Second Xiangya Hospital of Central South University, Changsha, China.
Bing XiaHunan Cancer Hospital, Changsha, China.
Yan ZhaoDepartment of Gynecology and Obstetrics, The Maternal and Child Health Hospital of Hunan Province, Changsha, China.
Qiaoyan LiDepartment of Gynecology and Obstetrics, The Third Xiangya Hospital of Central South University, Changsha, China.
Xiaoying WuDepartment of Pathology, Xiangya Hospital, Central South University, Changsha, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recently, an increasing number of studies have focused on the key function of long noncoding RNAs (lncRNAs) in biological activity. Abnormal lncRNA expression was found to relate to the development and pathogenesis of multiple cancers. LncRNA LINC00152 served as an oncogene in multiple cancers; however, its role in ovarian cancer remains unknown. In our research study, LINC00152 was upregulated in ovarian cancer tissues and cell lines. An increasing LINC00152 level was positively correlated with the histological grade, clinical stage, and poor prognosis of ovarian cancer patients. In addition, knockdown of LINC00152 reduced cell growth, induced cell apoptosis, and suppressed tumor growth. Moreover, we revealed that LINC00152 and Myeloid cell leukemia-1 (MCL-1) were targeted by miR-125b and had the same miR-125b combining site. The miR-125b level was negatively correlated with the expression of LINC00152, while MCL-1 was positively related to the LINC00152 level. MiR-125b could affect LINC00152 levels as evaluated by qRT-PCR. Finally, we affirmed that LINC00152 mediated cell proliferation by affecting MCL-1 expression and MCL-1-mediated mitochondrial apoptosis pathways and by working as a competitive endogenous RNA (ceRNA) of miR-125b. In summary, based on ceRNA theory, the combined research on miR-125b and MCL-1, and taking LINC00152 as a new study point, we provide new insight into the molecular mechanism of reversing cell proliferation in ovarian cancer.

Indexed as

Gene Expression Regulation, NeoplasticAdultAgedApoptosisCell Line, TumorCell MovementCell ProliferationFemaleGenes, ReporterHumansImmunohistochemistryMicroRNAsMiddle AgedMitochondriaMyeloid Cell Leukemia Sequence 1 ProteinNeoplasm Gradinglong non-coding RNA Linc00152, humanMCL1 protein, humanMicroRNAsMIRN125 microRNA, humanMyeloid Cell Leukemia Sequence 1 ProteinRNA, Long Noncodingcell proliferationcompetitive endogenous RNALINC00152long noncoding RNAMCL-1MiR-125bmitochondrial apoptosis pathwaysovarian cancer

Identifiers

PMID30030896
PMCPMC6144155

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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.