Evidence map›Paper›PMID 25118927›Full record

ArticleCell death & disease2014

Autophagy promotes paclitaxel resistance of cervical cancer cells: involvement of Warburg effect activated hypoxia-induced factor 1-α-mediated signaling.

X Peng, F Gong, Y Chen, Y Jiang, J Liu, M Yu, S Zhang, M Wang, G Xiao, H Liao

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed
7.9field-weighted citation impact, top 2% 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

84 citing papers in PubMed, 148 citations in OpenAlex.

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  12. Blockage of Autophagy for Cancer Therapy: A Comprehensive Review.International journal of molecular sciences · 2024
    Review
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24 more citing papers are in PubMed but not listed here.

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

10 authors at 5 institutions in 1 country.

X PengDepartment of Medical Oncology, Cancer Center, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu 610041, People's Republic of China.
F GongDepartment of Gynecology and Obstetrics, Second West China Hospital; and State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, Chengdu 610041, People's Republic of China.
Y ChenDepartment of Medical Oncology, Cancer Center, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu 610041, People's Republic of China.
Y JiangDepartment of Medical Oncology, Cancer Center, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu 610041, People's Republic of China.
J LiuDepartment of Medical Oncology, Cancer Center, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu 610041, People's Republic of China.
M YuDepartment of Medical Oncology, Cancer Center, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu 610041, People's Republic of China.
S ZhangDepartment of Medical Oncology, Cancer Center, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu 610041, People's Republic of China.
M WangCenter of Infectious Diseases, West China Hospital, Sichuan University, Chengdu 610041, People's Republic of China.
G XiaoDepartment of Pathology, Zunyi Medical College, Zunyi 563003, People's Republic of China.
H LiaoDepartment of Pathology, Wenzhou Central Hospital, Wenzhou 325000, People's Republic of China.
Sichuan University · CNState Key Laboratory of BiotherapyWenzhou Central Hospital · CNWest China Hospital of Sichuan University · CNZunyi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Paclitaxel is one of the most effective chemotherapy drugs for advanced cervical cancer. However, acquired resistance of paclitaxel represents a major barrier to successful anticancer treatment. In this study, paclitaxel-resistant HeLa sublines (HeLa-R cell lines) were established by continuous exposure and increased autophagy level was observed in HeLa-R cells. 3-Methyladenine or ATG7 siRNA, autophagy inhibitors, could restore sensitivity of HeLa-R cells to paclitaxel compared with parental HeLa cells. To determine the underlying molecular mechanism, differentially expressed proteins between HeLa and HeLa-R cells were identified by two-dimensional gel electrophoresis coupled with electrospray ionization quadrupole time-of-flight MS/MS. We found glycolysis-associated proteins were upregulated in HeLa-R cell lines. Inhibition of glycolysis by 2-deoxy-D-glucose or koningic acid could decrease autophagy and enhance sensitivity of HeLa-R cells to paclitaxel. Moreover, glycolysis could activate HIF1-α. Downregulation of HIF1-α by specific siRNA could decrease autophagy and resensitize HeLa-R cells to paclitaxel. Taken together, a possible Warburg effect activated HIF1-α-mediated signaling-induced autophagic pathway is proposed, which may provide new insight into paclitaxel chemoresistance.

Indexed as

AdenineAntineoplastic Agents, PhytogenicAutophagyAutophagy-Related Protein 7DeoxyglucoseDown-RegulationDrug Resistance, NeoplasmFemaleGlycolysisHeLa CellsHumansHypoxia-Inducible Factor 1, alpha SubunitMicrotubule-Associated ProteinsPaclitaxelRNA InterferenceSesquiterpenes3-methyladenineAdenineAntineoplastic Agents, PhytogenicATG7 protein, humanAutophagy-Related Protein 7Deoxyglucoseheptelidic acidHypoxia-Inducible Factor 1, alpha SubunitMAP1LC3A protein, humanMicrotubule-Associated ProteinsPaclitaxelSesquiterpenesUbiquitin-Activating Enzymes

Identifiers

PMID25118927
PMCPMC4454295
OpenAlexW2025291821

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.