Evidence map›Paper›PMID 28074102›Full record

ArticleEvidence-based complementary and alternative medicine : eCAM2016

Activation of p53/miR-34a Tumor Suppressor Axis by Chinese Herbal Formula JP-1 in A549 Lung Adenocarcinoma Cells.

Chih-Jung Yao, Jyh-Ming Chow, Pei-Chun Lin, Tsai-Shu Hu, Hui-Ching Kuo, Jhy-Shrian Huang, Kuan-Jen Bai, Gi-Ming Lai

Open access · hybridAbstract read
In one paragraph

Article in Evidence-based complementary and alternative medicine : eCAM, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.9field-weighted citation impact, top 21% 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

5 citing papers in PubMed, 12 citations in OpenAlex.

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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

8 authors at 3 institutions in 1 country.

Chih-Jung YaoCancer Center, Wan Fang Hospital, Taipei Medical University, Taipei 11696, Taiwan; Comprehensive Cancer Center of Taipei Medical University, Taipei 11031, Taiwan; Department of Internal Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taipei 11031, Taiwan.ORCID 0000-0001-6072-4033
Jyh-Ming ChowDepartment of Internal Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taipei 11031, Taiwan; Division of Hematology and Medical Oncology, Department of Internal Medicine, Wan Fang Hospital, Taipei Medical University, Taipei 11696, Taiwan.
Pei-Chun LinCancer Center, Wan Fang Hospital, Taipei Medical University, Taipei 11696, Taiwan.
Tsai-Shu HuCancer Center, Wan Fang Hospital, Taipei Medical University, Taipei 11696, Taiwan.
Hui-Ching KuoCancer Center, Wan Fang Hospital, Taipei Medical University, Taipei 11696, Taiwan.
Jhy-Shrian HuangComprehensive Cancer Center of Taipei Medical University, Taipei 11031, Taiwan.
Kuan-Jen BaiDivision of Pulmonary Medicine, Department of Internal Medicine, Wan Fang Hospital, Taipei Medical University, Taipei 11696, Taiwan; School of Respiratory Therapy, College of Medicine, Taipei Medical University, Taipei 11031, Taiwan.ORCID 0000-0001-8291-4436
Gi-Ming LaiCancer Center, Wan Fang Hospital, Taipei Medical University, Taipei 11696, Taiwan; Comprehensive Cancer Center of Taipei Medical University, Taipei 11031, Taiwan; Department of Internal Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taipei 11031, Taiwan; Division of Hematology and Medical Oncology, Department of Internal Medicine, Wan Fang Hospital, Taipei Medical University, Taipei 11696, Taiwan.ORCID 0000-0001-6123-8870
Taipei Medical University Hospital · TWWan Fang Hospital · TWTaipei Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer is the leading cause of cancer death worldwide; the most common pathologic type is lung adenocarcinoma (LADC). In spite of the recent progress in targeted therapy, most LADC patients eventually expired due to the inevitable recurrence and drug resistance. New complementary agent with evidence-based molecular mechanism is urgently needed. MiR-34a is an important p53 downstream tumor suppressor, which regulates apoptosis, cell-cycle, EMT (epithelial mesenchymal transition), and so forth. Its expression is deficient in many types of cancers including LADC. Here, we show that a Chinese herbal formula JP-1 activates p53/miR-34a axis in A549 human LADC cells (p53 wild-type). Treatment with JP-1 induces p53 and its downstream p21 and BAX proteins as well as the miR-34a, resulting in growth inhibition, colony formation reduction, migration repression, and apoptosis induction. Accordingly, the decreases of miR-34a downstream targets such as CDK6, SIRT1, c-Myc, survivin, Snail, and AXL were observed. Moreover, JP-1 activates AMPK

Identifiers

PMID28074102
PMCPMC5203917
OpenAlexW2565064944

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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.