Evidence map›Paper›PMID 27863492›Full record

ArticleJournal of biomedical science2016

Defective autophagy leads to the suppression of stem-like features of CD271

Dong Zhang, Qing Zhao, Hao Sun, Lijuan Yin, Jiajun Wu, Jun Xu, Tianxiang He, Chunlei Yang, Chengwei Liang

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of biomedical science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

36 citing papers in PubMed, 46 citations in OpenAlex.

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  20. A perspective on the role of autophagy in cancer.Biochimica et biophysica acta. Molecular basis of disease · 2021
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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

9 authors at 4 institutions in 1 country.

Dong ZhangDepartment of Spinal Disease, Yueyang Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, 200437, People's Republic of China.
Qing ZhaoDepartment of Spinal Disease, Yueyang Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, 200437, People's Republic of China.
Hao SunDepartment of Spinal Disease, Yueyang Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, 200437, People's Republic of China.
Lijuan YinDepartment of Pathology, Changhai Hospital, Second Military Medical University, Shanghai, People's Republic of China.
Jiajun WuDepartment of Spinal Disease, Yueyang Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, 200437, People's Republic of China.
Jun XuDepartment of Spinal Disease, Yueyang Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, 200437, People's Republic of China.
Tianxiang HeDepartment of Spinal Disease, Yueyang Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, 200437, People's Republic of China.
Chunlei YangDepartment of Spinal Disease, Yueyang Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, 200437, People's Republic of China. yangcl_yy@yeah.net.
Chengwei LiangDepartment of Orthopedics, Huadong Hospital Affiliated to Fudan University, No. 221 West Yan An Road, Shanghai, 200040, People's Republic of China. liang333cn@aliyun.com.
Yueyang Hospital · CNShanghai University of Traditional Chinese Medicine · CNChanghai Hospital · CNHuadong Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAs an important stress-response mechanism, autophagy plays crucial role in the tumor formation and drug resistance of cancer cells including osteosarcoma (OS). OS cancer stem cells (CSCs) also are considered a key factor of tumorigenesis, drug resistance and tumor recurrence. However, the relationship between autophagy and OS CSCs still remains unclear.

methodsCD271+ OS CSCs and CD271- OS cells were isolated by magnetic activated cell sorting. The autophagy level was evaluated by the mRNA expression of autophagy genes, the protein level of LC3II and p62, and the mean number of GFP-LC3 dot per cell. Lentivirus-delivered specific shRNA was utilized to inhibit the corresponding gene expression. The cell viability was examined with CCK8 assay. The cell proliferation level was detected with BrdU staining assay. Cell death was determined by Annexin V/PI double staining of fluorescence activated cell sorting, lactate dehydrogenase release and caspase-3 activity. Tumorigenicity ability was evaluated by colony and sphere formation assay, the protein expression of stemness markers and tumor formation in nude mice.

resultsOur data indicated that CD271+ OS CSCs had a similar basic autophagy level with CD271- OS cells. Autophagy deficiency had no observable effects on the levels of cell proliferation and death both in CD271+ and CD271- OS cells under normal condition. However, CD271+ OS cells showed a higher autophagy activity than CD271- OS cells under hypoxia and low nutrient (LH) condition. Moreover, autophagy-deficient CD271+ OS cells lost the advantage of tolerance to LH condition compared to CD271- OS cells. Meanwhile, autophagy deficiency enhanced the sensitivity to chemotherapeutics in the CD271+ cells to the comparable level in the CD271- cells. More importantly, deficient-autophagy decreased the protein expression of stemness markers and caused the disappearance of the superiority in tumorigenicity in vitro and vivo in CD271+ OS cells.

conclusionThe results above demonstrated that autophagy contributes to the stem-like features of CD271+ OS CSCs. Inhibition of autophagy is a promising strategy in the CSCs-targeting OS therapy.

Indexed as

AnimalsApoptosisAutophagyCarcinogenesisCell ProliferationGene Expression Regulation, NeoplasticHumansMiceMicrotubule-Associated ProteinsNeoplasm Recurrence, LocalNeoplastic Stem CellsNerve Tissue ProteinsOsteosarcomaProto-Oncogene Proteins c-mycReceptors, Nerve Growth FactorXenograft Model Antitumor AssaysMAP1LC3A protein, humanMicrotubule-Associated ProteinsNerve Tissue ProteinsNGFR protein, humanProto-Oncogene Proteins c-mycReceptors, Nerve Growth FactorAutophagyCancer stem cellsCD271Osteosarcoma

Identifiers

PMID27863492
PMCPMC5116184
OpenAlexW2555091877

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.