Evidence map›Paper›PMID 30108506›Full record

ArticleFrontiers in pharmacology2018

Lico A Causes ER Stress and Apoptosis via Up-Regulating miR-144-3p in Human Lung Cancer Cell Line H292.

Gang Chen, Yueping Ma, Zhe Jiang, Yuan Feng, Yueqing Han, Yetian Tang, Juan Zhang, Hui Ni, Xuezheng Li, Ning Li

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 6% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.

  1. Pooled it
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  7. Anticancer Potential of Natural Chalcones: In Vitro and In Vivo Evidence.International journal of molecular sciences · 2023
    Review
  8. [Licochalcone A induces cell cycle arrest in human lung squamous carcinoma cellsNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 5 institutions in 1 country.

Gang ChenSchool of Traditional Chinese Materia Medica, Shenyang Pharmaceutical University, Shenyang, China.
Yueping MaSchool of Traditional Chinese Materia Medica, Shenyang Pharmaceutical University, Shenyang, China.
Zhe JiangDepartment of Pharmacy, Affiliated Hospital of Yanbian University, Yanji, China.
Yuan FengSchool of Traditional Chinese Materia Medica, Shenyang Pharmaceutical University, Shenyang, China.
Yueqing HanSchool of Traditional Chinese Materia Medica, Shenyang Pharmaceutical University, Shenyang, China.
Yetian TangSchool of Traditional Chinese Materia Medica, Shenyang Pharmaceutical University, Shenyang, China.
Juan ZhangXinJiang Institute of Chinese Materia Medica and Ethnodrug, Ürümqi, China.
Hui NiXinJiang Institute of Chinese Materia Medica and Ethnodrug, Ürümqi, China.
Xuezheng LiDepartment of Pharmacy, Affiliated Hospital of Yanbian University, Yanji, China.
Ning LiSchool of Traditional Chinese Materia Medica, Shenyang Pharmaceutical University, Shenyang, China.
Guangxi Normal University · CNShenyang Pharmaceutical University · CNYanbian University Hospital · CNInstitute of Chinese Materia MedicaXinjiang Institute of Materia Medica · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During our study on the bioactivities of natural flavonoids, we found that the total flavonoids (TFs) and the main constituent of it, licochalcone A (lico A), activated unfolded protein response (UPR) and induced autophagy and thereby apoptosis in H292 cells. MicroRNAs, such as the tumor repressor miR-144-3p, were reported to be differentially expressed in lung cancer cells and were linked to ER stress, autophagy, and apoptosis. However, the underlying miRNA-based mechanism for lico A modulating proliferation, autophagy and apoptosis in lung cancer cells is elusive. In this study, we found that miR-144-3p was down-regulated in H292 cells comparing to normal embryonic lung cells WI-38, and lico A (10 μM) could increase miR-144-3p level in H292 cells. Knockdown of miR-144-3p significantly abrogated the apoptosis and proliferation-inhibiting effects of lico A, and lico A could enhance the proliferation-inhibiting effect and apoptosis induced by miR-144-3p overexpression. Moreover, overexpression miR-144-3p could induce ER stress by down-regulating Nrf2, and lico A enhanced the Nrf2 down-regulation caused by miR-144-3p overexpression. Co-transfection experiments showed that lico A potentially increased the dicing of pre-miR-144 so as to increase the mature miR-144-3p level. Interestingly, high level of lico A (40 μM) up-regulated CHOP protein, but failed to increase the downstream genes levels of CHOP, including Bim and Bcl-2 in H292 cells. Docking studies indicated that CHOP-mediated pathway was potentially blocked by high dose of lico A. Our results suggested that lico A could cause UPR, autophagy and apoptosis, and the underlying mechanism involved up-regulation of miR-144-3p, and increased lico A level would also increase the potential for lico A inhibiting CHOP-dependent apoptosis in H292 cells.

Indexed as

apoptosisautophagyCHOPdockinghomology modelingmiR-144-3p

Identifiers

PMID30108506
PMCPMC6079201
OpenAlexW2885764767

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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.