Evidence map›Paper›PMID 39588118›Full record

ArticleOpen life sciences2024

Combination effect of flavonoids attenuates lung cancer cell proliferation by inhibiting the STAT3 and FAK signaling pathway.

Pei Wan, Xingru Li, Shiqi Guo, Xiangling Zhao

Abstract read
In one paragraph

Article in Open life sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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

4 authors.

Pei WanDepartment of Thoracic and Cardiovascular Surgery, The First College of Clinical Medical Science, China Three Gorges University, Yichang Central People's Hospital, Yichang, Hubei, 443000, China.
Xingru LiDepartment of Respiratory and Critical Care Medicine, Lu'an People's Hospital of Anhui Province, Lu'an, Anhui, 237005, China.
Shiqi GuoDepartment of Thoracic and Cardiovascular Surgery, The First College of Clinical Medical Science, China Three Gorges University, Yichang Central People's Hospital, Yichang, Hubei, 443000, China.
Xiangling ZhaoDepartment of Respiratory and Critical Care Medicine, Lu'an People's Hospital of Anhui Province, Lu'an, Anhui, 237005, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer is considered the most ubiquitous malignant form of cancer, and the current treatment strategies do not offer effective outcomes to the patients. The present study examined the effectiveness of natural drugs delphinidin (DN) and oroxylin A (OA) in inhibiting the development of lung cancer cells (A549) through the blocking of the Signal transducer and activator of transcription 3 (STAT3) and focal adhesion kinase (FAK) intervene signaling pathways. These included cytotoxicity assessments, reactive oxygen species (ROS) levels, apoptotic morphological features, mitochondrial membrane potential (ΔΨm), nuclear fragmentation, and cell cycle analysis. Furthermore, the combination of DN and OA treatments on the expression of STAT-3, FAK, and various proliferation and apoptotic proteins was studied using western blotting. The results we have obtained are that the combination of DN and OA causes significant cytotoxicity, ROS, alteration of ΔΨm, and nuclear fragmentation, resulting in apoptosis of A549 cells. Furthermore, A549 cells treated with DN and OA concurrently displayed increased cell cycle arrest at the G2/M phase. Additionally, the combined DN and OA treatment inhibited the expression of STAT3 and FAK, suppressing proliferation and the induction of pro-apoptotic protein expressions in A549 cells. Thus, a combination of DN and OA could be used as a therapeutical approach to malignant forms of lung cancer.

Indexed as

cell proliferationdelphinidinlung canceroroxylin ASTAT3 and FAK

Identifiers

PMID39588118
PMCPMC11588013

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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.