Evidence map›Paper›PMID 26561201›Full record

SynthesisOncotarget2015

Tumor growth suppression by inhibiting both autophagy and STAT3 signaling in HNSCC.

Teng-Fei Fan, Lin-Lin Bu, Wei-Ming Wang, Si-Rui Ma, Jian-Feng Liu, Wei-Wei Deng, Liang Mao, Guang-Tao Yu, Cong-Fa Huang, Bing Liu and 2 more

RetractedOpen access · diamondAbstract readMeta-AnalysisRetracted Publication
In one paragraph

Synthesis in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

17 citing papers in PubMed, 30 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 1 institution in 1 country.

Teng-Fei Fan
Lin-Lin Bu
Wei-Ming Wang
Si-Rui Ma
Jian-Feng Liu
Wei-Wei Deng
Liang Mao
Guang-Tao Yu
Cong-Fa Huang
Bing Liu
Wen-Feng Zhang
Zhi-Jun Sun
Wuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is considered as a double-edged sword. It can prolong the survival of cancer cells and enhance its resistance to apoptosis, and paradoxically, defective autophagy has been linked to increased tumorigenesis, but the mechanism behind this phenomenon is unclear. In this study, we demonstrated that decreased phosphorylation of signal transducer and activator of transcription 3 (p-STAT3) was correlated with increased autophagy through the Akt/mTOR and Erk signaling pathways in human head and neck squamous cell carcinoma (HNSCC). We also showed that blockage of STAT3 by NSC74859 could markedly induce apoptotic cell death and autophagy. Meanwhile, increased autophagy inhibited apoptosis. The pharmacological or genetic inhibition of autophagy and STAT3 further sensitized HNSCC cells to apoptosis. Furthermore, evidence from xenograft model proved that suppressed STAT3 activity combined with inhibition of autophagy promoted tumor regression better than either treatment alone. Taken together, this present study demonstrated that autophagy alleviates apoptotic cell death in HNSCC, and combination of inhibition of STAT3 by NSC74859 and autophagy might be a promising new therapeutic strategy for HNSCC.

Indexed as

Aminosalicylic AcidsAnimalsAutophagyBenzenesulfonatesBlotting, WesternCarcinoma, Squamous CellCell Line, TumorCell ProliferationCluster AnalysisFemaleHead and Neck NeoplasmsHumansImmunohistochemistryMiceMice, Inbred BALB CPhosphorylationAminosalicylic AcidsBenzenesulfonatesNSC 74859STAT3 protein, humanSTAT3 Transcription Factorapoptosisautophagyhead and neck cancerSTAT3

Identifiers

PMID26561201
PMCPMC4791252
OpenAlexW2164137019

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.