Evidence map›Paper›PMID 29511449›Full record

ArticleAmerican journal of translational research2018

HDAC inhibitors suppressed small cell lung cancer cell growth and enhanced the suppressive effects of receptor-targeting cytotoxins via upregulating somatostatin receptor II.

Lichun Sun, Quanyong He, Cheguo Tsai, Jun Lei, Jing Chen, Lily Vienna Makcey, David H Coy

Abstract read
In one paragraph

Article in American journal of translational research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
–field-weighted citation impact
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

21 citing papers in PubMed.

  1. Review
  2. [Potential Mechanisms and Research Advances of HDAC1 in Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2026
    Review
  3. Article
  4. Entinostat Enhances the Efficacy of Chemotherapy in Small Cell Lung Cancer Through S-phase Arrest and Decreased Base Excision Repair.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
    Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Potential for Increasing Uptake of RadiolabeledCancer biotherapy & radiopharmaceuticals · 2021
    Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Regulatory Networks of LncRNA MALAT-1 in Cancer.Cancer management and research · 2020
    Review
  15. Review
  16. Article
  17. Epigenetics of lung cancer: a translational perspective.Cellular oncology (Dordrecht, Netherlands) · 2019
    Review
  18. Article
  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

7 authors.

Lichun SunThe Third Xiangya Hospital of Central South UniversityChangsha, China.
Quanyong HeThe Third Xiangya Hospital of Central South UniversityChangsha, China.
Cheguo TsaiDepartment of Medicine, School of Medicine, Tulane Health Sciences CenterNew Orleans, LA 70112-2699, USA.
Jun LeiThe Third Xiangya Hospital of Central South UniversityChangsha, China.
Jing ChenBusiness School, Hunan UniversityChangsha 410012, China.
Lily Vienna MakceyDepartment of Medicine, School of Medicine, Tulane Health Sciences CenterNew Orleans, LA 70112-2699, USA.
David H CoyDepartment of Medicine, School of Medicine, Tulane Health Sciences CenterNew Orleans, LA 70112-2699, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Small cell lung cancer (SCLC) is a malignant human cancer and patients have very limited benefit from traditional anticancer treatments, with a poor five-year survival rate being 10% less. In present study, we observed that Notch signalling activation induced SCLC cell growth suppression via overexpressing Notch active fragments (ICN1, ICN2, ICN3 and ICN4), implying its tumor suppressive role. The histone deacetylase (HDAC) inhibitors also displayed their suppressive effects. Valproic acid (VPA) as a HDAC inhibitor was found to suppress SCLC cell growth and cell cycle arrest at phase G1, and observed to decrease HDAC4 and increase acetylation of histone H4 (AcH4) while activating Notch signalling with an increase of Notch1, Notch target gene HES1 and p21. Meanwhile, we also observed that VPA greatly stimulated the expression of somatostatin receptor type II (SSTR2) that is usually overexpressed in many cancer cells and is used as a target for anticancer drug development, providing a combination therapy with VPA and the SSTR2-targeting cytotoxins. Thus, VPA was investigated in combination with SSTR2-targeted cytotoxins captothecine-somatostatin conjugate (CPT-SST) and colchicine-somatostatin conjugate (COL-SST). Our assays showed that these combination treatments strongly led to a greater suppression as compared to each alone. In conclusion, we found that VPA suppressed SCLC cell growth and increased the expression of SSTR2. These may provide a novel clinical opportunity for enhanced anticancer therapy using the combination strategy of Notch signalling regulator and SSTR2-targeting cytotoxins in SCLC treatments.

Indexed as

cell proliferationHDAC inhibitorNotch signalingSmall cell lung cancersomatostatin receptorvalproic acid

Identifiers

PMID29511449
PMCPMC5835820

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.