Evidence map›Paper›PMID 33194045›Full record

ArticleAmerican journal of translational research2020

Caspase-8 knockdown suppresses apoptosis, while induces autophagy and chemo-sensitivity in non-small cell lung cancer cells.

Hui Zuo, Cheng Chen, Ling Ma, Qiu-Xia Min, Yue-Hai Shen

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

7 citing papers in PubMed, 9 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

5 authors at 2 institutions in 1 country.

Hui ZuoDepartment of Pharmacology, The First People's Hospital of Yunnan Province Kunming 650032, Yunnan Province, China.
Cheng ChenDepartment of Pharmacology, The First People's Hospital of Yunnan Province Kunming 650032, Yunnan Province, China.
Ling MaDepartment of Pharmacology, The First People's Hospital of Yunnan Province Kunming 650032, Yunnan Province, China.
Qiu-Xia MinDepartment of Pharmacology, The First People's Hospital of Yunnan Province Kunming 650032, Yunnan Province, China.
Yue-Hai ShenFaculty of Life Science and Technology, Kunming University of Science and Technology Kunming 655034, Yunnan Province, China.
Kunming University of Science and Technology · CNFirst People's Hospital of Yunnan Province · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeDrug resistance remains a major cause of relapse and therapeutic failure in non-small cell lung cancer (NSCLC). The purpose of this investigation is to explore the relationship between caspase-8 level and chemo-sensitivity, as well as its underlying mechanism in NSCLC cells.

methodsNSCLC cell line, A549 cells was used to investigate the influence of caspase-8 on the biological behavior

resultsOur results indicated that cells infected with sh-caspase-8 exhibited high knockdown efficiency. Knockdown of caspase-8 significantly reduced apoptosis of A549 cells. As evidenced by the decreased number of apoptotic cells and the reduction of Bcl-2/bax ratio. Interestingly, caspase-8 knockdown also enhanced autophagy in A549 cells. Additionally, knockdown of caspase-8 reduced the doxorubicin, carboplatin, cisplatin, and etoposide sensitivity towards A549 cells.

conclusionIn summary, our results revealed that knockdown of caspase-8 could promote cell growth and autophagy, while reduce chemo-sensitivity and apoptotic cell death. These finding suggest caspase-8 might serve as a potential target to improve the chemo-sensitivity for NSCLC patients in clinical setting.

Indexed as

apoptosisautophagyCaspase-8chemo-sensitivityNSCLC

Identifiers

PMID33194045
PMCPMC7653624
OpenAlexW3100234574

What OpenQuestion holds

Textmetadata
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Registered trials

None linked

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.