Evidence map›Paper›PMID 30741368›Full record

ArticleMolecular and cellular biochemistry2019

LCAL1 enhances lung cancer survival via inhibiting AMPK-related antitumor functions.

Jun-Yu Li, Zhi-Qiang Luo

Abstract read
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In one paragraph

Article in Molecular and cellular biochemistry, 2019. 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
–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

14 citing papers in PubMed.

  1. Review
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  12. Molecular therapy. Nucleic acids · 2020
    Article
  13. Regulation of Autophagy by Glycolysis in Cancer.Cancer management and research · 2020
    Review
  14. 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

2 authors.

Jun-Yu LiDepartment of Oncology, Jiangxi Cancer Hospital, No. 519 Beijing East Road, Nanchang, 330029, Jiangxi, People's Republic of China.
Zhi-Qiang LuoDepartment of Oncology, Jiangxi Cancer Hospital, No. 519 Beijing East Road, Nanchang, 330029, Jiangxi, People's Republic of China. Lzqiang87@gmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer is one of the most common cancers and has been the most common cause of cancer deaths for several decades. Recently, lung cancer-associated lncRNA 1 (LCAL1) has been identified to be overexpressed in lung cancer tissues, while inhibiting LCAL1 expression has shown potential to inhibiting lung cancer growth. However, the molecular mechanism between LCAL1 and lung cancer cell survival remains poorly understood. In the present study, we provided the first evidence that LCAL1 may support lung cancer survival via inhibiting the activity of AMP-activated protein kinase (AMPK). According to our results, LCAL1 may physically interact with the catalytic subunit of tumor suppressor AMPK, prevent AMPK activation by upstream kinase (liver kinase B1), and thus inhibit the downstream AMPK signaling network. Our study revealed that overexpressed LCAL1 may induce aerobic glycolysis in lung cancer cells through AMPK/HIF1α axis, enhance protein synthesis through AMPK/mTOR/S6K axis, and suppress autophagic cell death through AMPK/ULK1 pathway. All these alterations supported rapid proliferation of lung cancer cells, while knockdown of LCAL1 expression demonstrated the potential of inhibiting lung cancer growth by reversing the tumorigenic phenotypes triggered by the loss of AMPK activity, and could become a promising therapeutic strategy for lung cancer treatment.

Indexed as

AgedAged, 80 and overAMP-Activated Protein KinasesAutophagyCarcinoma, Non-Small-Cell LungCell Line, TumorDisease-Free SurvivalEnzyme ActivationFemaleHumansLung NeoplasmsMaleMiddle AgedNeoplasm ProteinsRNA, Long NoncodingRNA, NeoplasmAMP-Activated Protein KinasesMTOR protein, humanNeoplasm ProteinsRNA, Long NoncodingRNA, NeoplasmTOR Serine-Threonine KinasesAMPKLCAL1LncRNALung cancer

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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.