Evidence map›Paper›PMID 32257917›Full record

ArticleLaboratory animal research2019

Inhibition of STAT3 signaling induces apoptosis and suppresses growth of lung cancer: good and bad.

Ju-Hee Kang, Yeong-Su Jang, Ha Jung Lee, Chang-Yong Lee, Dong Yun Shin, Seung Hyun Oh

Open access · diamondAbstract read
In one paragraph

Article in Laboratory animal research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.0field-weighted citation impact, top 11% 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

25 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Anticancer Effects ofInternational journal of molecular sciences · 2026
    Article
  3. Article
  4. Cellular signaling meets bacterial infection: the integrative role of STAT3.Frontiers in cellular and infection microbiology · 2026
    Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Targeting STAT3 Enzyme for Cancer Treatment.Mini reviews in medicinal chemistry · 2024
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  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

6 authors at 1 institution in 1 country.

Ju-Hee Kang *College of Pharmacy, Gachon University, Incheon, Republic of Korea.
Yeong-Su Jang *College of Pharmacy, Gachon University, Incheon, Republic of Korea.
Ha Jung LeeCollege of Pharmacy, Gachon University, Incheon, Republic of Korea.
Chang-Yong LeeCollege of Pharmacy, Gachon University, Incheon, Republic of Korea.
Dong Yun ShinCollege of Pharmacy, Gachon University, Incheon, Republic of Korea.
Seung Hyun OhCollege of Pharmacy, Gachon University, Incheon, Republic of Korea.ORCID 0000-0003-3678-2772
Gachon University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Signal transducer and activator of transcription 3 (STAT3) modulates a variety of genes involved in the regulation of critical functions, including cell proliferation, differentiation, apoptosis, angiogenesis, metastasis, and immunity. For many cancers, elevated levels of STAT3 signaling have been associated with a poor prognosis and the development of chemotherapy resistance. In this study, we investigated the inhibitory effects of a novel small-molecule inhibitor of STAT3, STX-0119, on the cell viability and survival of human lung cancer cells. STX-0119 inhibited activated STAT3 and the expression of STAT3-regulated oncoproteins such as c-Myc, cyclin D1, and survivin in lung cancer cells. STX-0119 also decreased the amount of STAT3 in the nuclear fraction as well as induced apoptosis of these lung cancer cell lines as evidenced by increases in apoptotic cells (Annexin V positive) and poly (ADP-ribose) polymerase (PARP) cleavage. The efficacy of STX-0119 in a mouse xenograft model was confirmed. However, a hematological side effect, which had not been previously reported, was observed. The level of white blood cells was significantly lowered when treated at the dose at which STX-0119 alone showed a significant tumor-suppressive effect. In conclusion, we suggest that STX-0119 may be a potent therapeutic agent against lung cancer. Consideration of the side effect suggests, it is necessary to study whether low-dose STX-0119 is effective for lung treatment with a combination of classic lung cancer therapeutics.

Indexed as

CancerNSCLCSTAT3 inhibitorSTX-0119Xenograft

Identifiers

PMID32257917
PMCPMC7081529
OpenAlexW2995571090

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.