Evidence map›Paper›PMID 26794658›Full record

ArticleCell death & disease2016

Targeting HDAC with a novel inhibitor effectively reverses paclitaxel resistance in non-small cell lung cancer via multiple mechanisms.

L Wang, H Li, Y Ren, S Zou, W Fang, X Jiang, L Jia, M Li, X Liu, X Yuan and 3 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 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
6.6field-weighted citation impact, top 3% 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

52 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. HDAC-driven mechanisms in anticancer resistance: epigenetics and beyond.Cancer drug resistance (Alhambra, Calif.) · 2024
    Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Differential molecular mechanistic behavior of HDACs in cancer progression.Medical oncology (Northwood, London, England) · 2022
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Nanomedicine Strategies for Management of Drug Resistance in Lung 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

13 authors at 2 institutions in 1 country.

L WangDepartment of Pharmacology, Shenyang Pharmaceutical University, Shenyang, PR China.
H LiDepartment of Pharmacology, Shenyang Pharmaceutical University, Shenyang, PR China.
Y RenDepartment of Pathology, Wuhan General Hospital of Guangzhou Command, People's Liberation Army, Wuhan, PR China.
S ZouKey Laboratory of Structure-Based Drugs Design and Discovery of Ministry of Education, Shenyang Pharmaceutical University, Shenyang, PR China.
W FangKey Laboratory of Structure-Based Drugs Design and Discovery of Ministry of Education, Shenyang Pharmaceutical University, Shenyang, PR China.
X JiangDepartment of Pharmacology, Shenyang Pharmaceutical University, Shenyang, PR China.
L JiaDepartment of Pharmacology, Shenyang Pharmaceutical University, Shenyang, PR China.
M LiDepartment of Pharmacology, Shenyang Pharmaceutical University, Shenyang, PR China.
X LiuDepartment of Pharmacology, Shenyang Pharmaceutical University, Shenyang, PR China.
X YuanDepartment of Pharmacology, Shenyang Pharmaceutical University, Shenyang, PR China.
G ChenKey Laboratory of Structure-Based Drugs Design and Discovery of Ministry of Education, Shenyang Pharmaceutical University, Shenyang, PR China.
J YangDepartment of Pharmacology, Shenyang Pharmaceutical University, Shenyang, PR China.
C WuDepartment of Pharmacology, Shenyang Pharmaceutical University, Shenyang, PR China.
Shenyang Pharmaceutical University · CNWuhan General Hospital of Guangzhou · CN

Funding

Mechanisms of Alcohol Hangover HeadacheR21AA020305 · NIAAA · BETH ISRAEL DEACONESS MEDICAL CENTER · PI LEVY, DAN · 2012 to 2013
$442k
NIAAA NIH HHS R21 AA020305
6 · The paper itself

Abstract

Chemotherapy paclitaxel yields significant reductions in tumor burden in the majority of advanced non-small cell lung cancer (NSCLC) patients. However, acquired resistance limits its clinical use. Here we demonstrated that the histone deacetylase (HDAC) was activated in paclitaxel-resistant NSCLC cells, and its activation promoted proliferation and tumorigenesis of paclitaxel-resistant NSCLC cells in vitro and in vivo. By contrast, knockdown of HDAC1, a primary isoform of HDAC, sensitized resistant cells to paclitaxel in vitro. Furthermore, we observed that overexpression of HDAC1 was associated with the downregulation of p21, a known HDAC target, in advanced NSCLC patients with paclitaxel treatment, and predicted chemotherapy resistance and bad outcome. In addition, we also identified a novel HDACs inhibitor, SNOH-3, which inhibited HDAC expression and activity, induced cell apoptosis, and suppressed cell migration, invasion and angiogenesis. Notably, co-treatment with SNOH-3 and paclitaxel overcome paclitaxel resistance through inhibiting HDAC activity, leading to the induction of apoptosis and suppression of angiogenesis in vitro and in preclinical model. In summary, our data demonstrate a role of HDAC in paclitaxel-resistant NSCLC and provide a promising therapeutic strategy to overcome paclitaxel-acquired resistance.

Indexed as

Carcinoma, Non-Small-Cell LungHistone DeacetylasesHumansLung NeoplasmsPaclitaxelHistone DeacetylasesPaclitaxel

Identifiers

PMID26794658
PMCPMC4816165
OpenAlexW2412362928

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.