Evidence map›Paper›PMID 30122943›Full record

ArticleOncoTargets and therapy2018

Melittin induces NSCLC apoptosis via inhibition of miR-183.

Dongqi Gao, Jingjing Zhang, Lu Bai, Fubo Li, Yi Dong, Qingshan Li

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

14 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Review
  3. A Comparative Study of Melittins fromInternational journal of molecular sciences · 2025
    Article
  4. Intrinsic apoptotic effect of Anatolian honeybee (Turkish journal of biology = Turk biyoloji dergisi · 2025
    Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
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  13. Article
  14. Melittin suppresses growth and induces apoptosis of non-small-cell lung cancer cells via down-regulation of TGF-β-mediated ERK signal pathway.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2020
    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.

Dongqi GaoDepartment of Oncology, Affiliated Hospital of Chengde Medical University, Chengde 067000, China, qingshan_ql@126.com.
Jingjing ZhangDepartment of Oncology, Affiliated Hospital of Chengde Medical University, Chengde 067000, China, qingshan_ql@126.com.
Lu BaiDepartment of Oncology, Affiliated Hospital of Chengde Medical University, Chengde 067000, China, qingshan_ql@126.com.
Fubo LiDepartment of Oncology, Affiliated Hospital of Chengde Medical University, Chengde 067000, China, qingshan_ql@126.com.
Yi DongDepartment of Oncology, Affiliated Hospital of Chengde Medical University, Chengde 067000, China, qingshan_ql@126.com.
Qingshan LiDepartment of Oncology, Affiliated Hospital of Chengde Medical University, Chengde 067000, China, qingshan_ql@126.com.
Chengde Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNon-small-cell lung cancer (NSCLC) has one of the highest mortality rates among cancers worldwide, with a poor prognosis. Previous studies have reported that melittin, an active component of apitoxin, exerts anti-inflammatory and antitumor effects via vascular endothelial growth factor or FoxO1.

methodsCCK8, flow cytometry assay and Western blotting were performed to evaluate the effect of melittin on NSCLC.

resultsThe present study demonstrates that melittin activated caspase-2 by inhibiting miR-183 expression and, thus, induced NSCLC apoptosis in both NCI-H441 cancer cell line assays and an in vivo xenograft model. The results of the cell-based assays showed that melittin (2 μg/mL) robustly suppressed miR-183 expression level and resulted in decreased invasion and migration abilities of NCI-H441 cells. Additionally, a flow cytometry assay and Western blotting showed that melittin induced NSCLC NCI-H441 cell apoptosis along with significant elevation of caspase-2 and Bax, which are regulators of cell apoptosis, and reduced Bcl-2 protein expression compared with dimethyl sulfoxide control. Furthermore, subcutaneous injection of melittin (5 mg/kg) significantly suppressed NSCLC tumor growth compared with vehicle group tumors, determined through tumor size and weight.

conclusionTaken together, the aforementioned findings contribute to identification of a novel therapeutic target in the treatment of NSCLC, in patients diagnosed with a high expression of miR-183. Moreover, this article provides solid evidence for the inhibitory effect of melittin on NSCLC cancer cell growth.

Indexed as

apoptosiscaspase 2melittinmiR-183NSCLC

Identifiers

PMID30122943
PMCPMC6078185
OpenAlexW2885329915

What OpenQuestion holds

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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.