Evidence map›Paper›PMID 30849960›Full record

ArticleBMC cancer2019

MicroRNA-148b regulates tumor growth of non-small cell lung cancer through targeting MAPK/JNK pathway.

Lin Lu, Qiyao Liu, Peipei Wang, Yong Wu, Xia Liu, Chengyin Weng, Xisheng Fang, Baoxiu Li, Xiaofei Cao, Haibo Mao and 4 more

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

17 citing papers in PubMed, 31 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

14 authors at 3 institutions in 1 country.

Lin LuDepartment of Medical Oncology, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, 510180, Guangdong, China.
Qiyao LiuDepartment of Medical Oncology, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, 510180, Guangdong, China.
Peipei WangDepartment of Medical Oncology, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, 510180, Guangdong, China.
Yong WuDepartment of Medical Oncology, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, 510180, Guangdong, China.
Xia LiuDepartment of Medical Oncology, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, 510180, Guangdong, China.
Chengyin WengDepartment of Medical Oncology, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, 510180, Guangdong, China.
Xisheng FangDepartment of Medical Oncology, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, 510180, Guangdong, China.
Baoxiu LiDepartment of Medical Oncology, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, 510180, Guangdong, China.
Xiaofei CaoDepartment of Medical Oncology, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, 510180, Guangdong, China.
Haibo MaoDepartment of Medical Oncology, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, 510180, Guangdong, China.
Lina WangDepartment of Medical Oncology, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, 510180, Guangdong, China.
Mingmei GuanDepartment of Medical Oncology, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, 510180, Guangdong, China. 13808815499@163.com.
Wei WangDepartment of Experimental Research and State Key Laboratory of Oncology in Southern China, Sun Yat-Sen University Cancer Center, Guangzhou, 510080, Guangdong, China. wangwei@sysucc.org.cn.
Guolong LiuDepartment of Medical Oncology, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, 510180, Guangdong, China. eyglliu@scut.edu.cn.ORCID http://orcid.org/0000-0001-7391-8750
Guangzhou First People's Hospital · CNFirst Affiliated Hospital of Guangzhou Medical University · CNSun Yat-sen University · CN

Funding

Fundamental Research Funds for the Central Universities x2xy-D2175050National Natural Science Foundation of China 81502563National Natural Science Foundation of China 81672900Natural Science Foundation of Guangdong Province 2016A030310109Science and Technology Program of Guangzhou 201707010262
6 · The paper itself

Abstract

backgroundMicroRNA-148b (miR-148b) has been detected in various types of tumors, and is generally viewed as a tumor suppressor. Our previous study found the decreased expression of miR-148b in human non small cell lung cancer (NSCLC) specimens and cell lines. However, the underlying mechanisms of miR-148b in regulating tumor progression remain unclear.

methodsFirstly animal experiments were performed to verify whether miR-148b could inhibit the tumor growth. Then, the underlying mechanisms were studied by transfecting recombinant plasmids containing a miR-148b mimic or a negative control (NC) mimic (shRNA control) into NSCLC cell lines PC14/B and A549 cells. Tumor cells transfected with unpackaged lentiviral vectors was used as blank control. Cell proliferation capabilities were measured by using CCK-8 kit and colony formation assay. Cell cycle arrest was compared to clarify the mechanism underlying the tumor cell proliferation. Annexin V-FITC Apoptosis Detection kit was applied to investigate the effect of miR-148b on cell apoptosis. Furthermore, western blot analysis were performed to study the targeting pathway.

resultsWe found that over-expression of miR148b could significantly inhibit tumor growth, while knocking down miR148b could obviously promote tumor growth. Further experiment showed that miR-148b inhibited tumor cell proliferation. Besides, over-expression of miR148b decreased the G2/M phase population of the cell cycle by preventing NSCLC cells from entering the mitotic phase and enhanced tumor cell apoptosis. Further western blot analysis indicated that miR148b could inhibit mitogen-activated protein kinase/Jun N-terminal kinase (MAPK/JNK) signaling by decreasing the expression of phosphorylated (p) JNK.

conclusionsThese results demonstrate that miR-148b could inhibit the tumor growth and act as tumor suppressor by inhibiting the proliferation and inducing apoptosis of NSCLC cells by blocking the MAPK/JNK pathway.

Indexed as

Gene Expression Regulation, NeoplasticMAP Kinase Signaling SystemAnimalsApoptosisCarcinoma, Non-Small-Cell LungCell Cycle CheckpointsCell Line, TumorCell ProliferationDisease Models, AnimalFemaleHumansLung NeoplasmsMiceMicroRNAsPhosphorylationRNA InterferenceMicroRNAsMIRN148 microRNA, humanApoptosisMAPK/JNK pathwaymicroRNA-148bNon small cell lung cancer (NSCLC);tumor suppressorProliferation

Identifiers

PMID30849960
PMCPMC6408859
OpenAlexW2941511722

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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.