Evidence map›Paper›PMID 26962687›Full record

ArticleCell death & disease2016

MiR-125a-5p decreases after long non-coding RNA HOTAIR knockdown to promote cancer cell apoptosis by releasing caspase 2.

L Tang, H Shen, X Li, Z Li, Z Liu, J Xu, S Ma, X Zhao, X Bai, M Li and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 6% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Critical role of HOX transcript antisense intergenic RNA (HOTAIR) in gliomas.Journal of molecular medicine (Berlin, Germany) · 2020
    Review
  9. Article
  10. Review
  11. Long Chain Non-Coding RNA (lncRNA) HOTAIR Knockdown Increases miR-454-3p to Suppress Gastric Cancer Growth by Targeting STAT3/Cyclin D1.Medical science monitor : international medical journal of experimental and clinical research · 2019
    Article
  12. Article
  13. Article
  14. MiR-125a-5p promotes osteoclastogenesis by targeting TNFRSF1B.Cellular & molecular biology letters · 2019
    Article
  15. Review
  16. miRNA Signature in NAFLD: A Turning Point for a Non-Invasive Diagnosis.International journal of molecular sciences · 2018
    Review
  17. Interaction and cross-talk between non-coding RNAs.Cellular and molecular life sciences : CMLS · 2018
    Review
  18. The long noncoding RNAThe Journal of biological chemistry · 2017
    Article
  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

12 authors at 5 institutions in 1 country.

L TangState Key Laboratory of Protein and Plant Gene Research, College of Life Sciences, Peking University, Beijing, China.
H ShenKey Laboratory of Genomics and Precision Medicine, China Gastrointestinal Cancer Research Center, Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing, China.
X LiState Key Laboratory of Protein and Plant Gene Research, College of Life Sciences, Peking University, Beijing, China.
Z LiState Key Laboratory of Protein and Plant Gene Research, College of Life Sciences, Peking University, Beijing, China.
Z LiuInstitute of Forensic Science, Ministry of Public Security, Beijing, China.
J XuInstitute of Forensic Science, Ministry of Public Security, Beijing, China.
S MaState Key Laboratory of Protein and Plant Gene Research, College of Life Sciences, Peking University, Beijing, China.
X ZhaoState Key Laboratory of Protein and Plant Gene Research, College of Life Sciences, Peking University, Beijing, China.
X BaiState Key Laboratory of Protein and Plant Gene Research, College of Life Sciences, Peking University, Beijing, China.
M LiDepartment of General Surgery, Beijing ChaoYang Hospital, Capital University of Medical Sciences, Beijing, China.
Q WangState Key Laboratory of Protein and Plant Gene Research, College of Life Sciences, Peking University, Beijing, China.
J JiState Key Laboratory of Protein and Plant Gene Research, College of Life Sciences, Peking University, Beijing, China.
Peking University · CNBeijing Chao-Yang Hospital · CNBeijing Institute of Genomics · CNInstitute of Forensic Science · CNMinistry of Public Security of the People's Republic of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

HOTAIR (homeobox transcript antisense RNA), one of the prototypical long non-coding RNAs, has been verified overexpressed in multiple carcinomas and has emerged as a promising novel anticancer target. Its well-established role is acting as a predictor of poor prognosis and promoting cancer cell metastasis. Recently, another important mission of HOTAIR was uncovered that targeting HOTAIR caused cancer cell apoptosis. Nevertheless, so far there is no published data elaborating the mechanism. Here, we report that microRNA miR-125a-5p decreases and releases caspase 2 to promote cancer cell apoptosis after HOTAIR knockdown. We applied siRNAs targeting HOTAIR to various cancer cells, and observed apoptosis in all of these cell lines. RNA sequencing detected that miR-125a-5p was decreased after HOTAIR knockdown and miR-125a-5p mimics could rescue the apoptosis induced by HOTAIR deficiency. Luciferase assays identified caspase 2, an initiator caspase, to be a new target of miR-125a-5p. Elevated expression and subsequent cleavage of caspase 2 was observed after HOTAIR knockdown or inhibition of miR-125a-5p. RNAi of caspase 2 could attenuate the apoptosis induced by HOTAIR knockdown. In 80 clinical colon cancer tissues, HOTAIR and miR-125a-5p levels were higher than adjacent tissues, whereas caspase 2 was lower. MiR-125a-5p expression level was significantly correlated with colon tumor size, lymph node metastasis and clinical stage. These findings indicate that miR-125a-5p decreases after HOTAIR knockdown to promote cancer cell apoptosis by releasing caspase 2. Our work reveals a previously unidentified apoptotic mechanism, which might be exploitable in anticancer drug development.

Indexed as

ApoptosisCaspase 2Cysteine EndopeptidasesGene Knockdown TechniquesHeLa CellsHumansMicroRNAsNeoplasm ProteinsNeoplasmsRNA, Long NoncodingRNA, NeoplasmCASP2 protein, humanCaspase 2Cysteine EndopeptidasesHOTAIR long untranslated RNA, humanMicroRNAsMIRN125 microRNA, humanNeoplasm ProteinsRNA, Long NoncodingRNA, Neoplasm

Identifiers

PMID26962687
PMCPMC4823942
OpenAlexW2293941224

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.