Evidence map›Paper›PMID 26526583›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016

Rapamycin inhibited the function of lung CSCs via SOX2.

Li-Xia Xie, Feng-Feng Sun, Bin-Feng He, Xiao-Feng Zhan, Juan Song, Sheng-Song Chen, Shi-Cang Yu, Xiao-Qun Ye

Abstract read
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In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

5 citing papers in PubMed, 14 citations in OpenAlex.

  1. Co-delivery of SN38 and rapamycin albumin bound nanoparticles against breast Cancer.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2025
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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

8 authors at 4 institutions in 1 country.

Li-Xia XieDepartment of Respiratory Diseases, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, China.
Feng-Feng SunDepartment of Respiratory Diseases, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, China.
Bin-Feng HeTranslational Research Center, North Sichuan Medical College, Nanchong, Sichuan, 637000, People's Republic of China.
Xiao-Feng ZhanDepartment of Respiratory Diseases, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, China.
Juan SongDepartment of Respiratory Diseases, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, China.
Sheng-Song ChenDepartment of Respiratory Diseases, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, China.
Shi-Cang YuInstitute of Pathology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University, Chongqing, 400037, China.
Xiao-Qun YeDepartment of Respiratory Diseases, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, China. xqyencu@gmail.com.
Nanchang University · CNSecond Affiliated Hospital of Nanchang University · CNNorth Sichuan Medical University · CNSouthwest Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The presence of cancer stem cells (CSCs) is the source of occurrence, aggravation, and recurrence of lung cancer. Accordingly, targeting killing the lung CSCs has been suggested to be an effective approach for lung cancer treatment. In this study, we showed that rapamycin inhibited the mammalian target of rapamycin (mTOR) signal transduction in A549 cells and improved the sensitivity to cisplatin (DDP). The mechanisms involve inhibition of the SOX2 expression, cell proliferation, epithelial-mesenchymal transition (EMT) phenotype, and sphere formation. Interestingly, knocked down SOX2 was a similar effect with rapamycin in A549 sphere. Furthermore, we showed that ectopic expression of Sox2 in A549 cells was sufficient to render them more resistant to rapamycin treatment in vitro. These data suggested that rapamycin inhibited the function of lung CSCs via SOX2. It will be of great interest to further explore the therapeutic strategies of lung cancer.

Indexed as

Cell Line, TumorCell ProliferationCisplatinDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionHumansLung NeoplasmsNeoplasm Recurrence, LocalNeoplastic Stem CellsSirolimusSOXB1 Transcription FactorsCisplatinSirolimusSOX2 protein, humanSOXB1 Transcription FactorsCancer stem cellLung cancermTORRapamycinSOX2

Identifiers

PMID26526583
OpenAlexW1950635678

What OpenQuestion holds

Textmetadata
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.