Evidence map›Paper›PMID 27508098›Full record

ArticleAmerican journal of cancer research2016

MiR-153 promotes breast cancer cell apoptosis by targeting HECTD3.

Xiaowei Wu, Lin Li, Yi Li, Zhihua Liu

Open access · greenAbstract read
In one paragraph

Article in American journal of cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.4field-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

30 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Angioregulatory microRNAs in breast cancerJournal of advanced research · 2022
    Review
  8. Review
  9. Article
  10. The role of E3 ubiquitin ligase HECTD3 in cancer and beyond.Cellular and molecular life sciences : CMLS · 2020
    Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Observational
  16. Article
  17. Review
  18. Article
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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

4 authors at 1 institution in 1 country.

Xiaowei WuState Key Laboratory of Molecular Oncology, National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College Beijing, 100021, China.
Lin LiState Key Laboratory of Molecular Oncology, National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College Beijing, 100021, China.
Yi LiState Key Laboratory of Molecular Oncology, National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College Beijing, 100021, China.
Zhihua LiuState Key Laboratory of Molecular Oncology, National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College Beijing, 100021, China.
Chinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Homologous to the E6-associated protein carboxyl terminus domain containing 3 (HECTD3) is an E3 ubiquitin ligase which ubiquitinates caspase-8, caspase-9 and promotes cancer cell survival. Aberrant HECTD3 expression is frequently involved in various types of cancer progression. However, to date, the regulation of HECTD3 remains unclear. Here, we demonstrated that miR-153 functions as a negative regulator of HECTD3 and sensitizes cisplatin-induced apoptosis in triple-negative breast cancer cells MDA-MB-231 and BT-549. Luciferase reporter assay demonstrated that miR-153 suppresses HECTD3 expression through directly targeting its mRNA within the 3'-Untranslated Region (3'UTR). Additionally, the expression levels of miR-153 and HECTD3 are inversely correlated in breast cancer cell lines. Furthermore, ectopic expression of miR-153 promotes apoptosis in MDA-MB-231 and BT-549 cells treated with cisplatin or TNF-α, and miR-153 inhibitor treatment inhibits cisplatin induced apoptosis in MDA-MB-231 and BT-549 cells. Moreover, stable overexpression of HECTD3 abrogates the sensitization effect of miR-153 to cisplatin treatment in MDA-MB-231 cells, and miR-153 inhibitor protects cells against cisplatin cytotoxicity in control cells, but not in the stable knockdown HECTD3 MDA-MB-231 cells. More importantly, breast cancer patients with higher expression levels of miR-153 had significant higher 5-year survival rate in PROGmiR database (P<0.05). Taken together, our study indicated that miR-153 inhibits TNBC survival by targeting HECTD3 and functions as a potent tumor suppressor.

Indexed as

apoptosisHECTD3miR-153

Identifiers

PMID27508098
PMCPMC4969405
OpenAlexW2507671758

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.