Evidence map›Paper›PMID 23589145›Full record

ArticleDigestive diseases and sciences2013

Insulin-like growth factor 1 receptor promotes the growth and chemoresistance of pancreatic cancer.

Xiaodong Tian, Kun Hao, Changfu Qin, Kun Xie, Xuehai Xie, Yinmo Yang

Abstract read
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In one paragraph

Article in Digestive diseases and sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-weighted citation impact, top 19% 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, 26 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

6 authors at 2 institutions in 1 country.

Xiaodong TianDepartment of General Surgery, Peking University First Hospital, 8th Xishiku Street, Xicheng District, Beijing, 100034, People's Republic of China.
Kun Hao
Changfu Qin
Kun Xie
Xuehai Xie
Yinmo Yang
Peking University · CNPeking University First Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInsulin-like growth factor 1 receptor (IGF1R) plays important roles in the progression of pancreatic cancer. However, the underlying mechanism remains unclear.

aimsThe purpose of this study was to investigate the effects of IGF1R knockdown on the proliferation, apoptosis and chemosensitivity of pancreatic cancer cells, and explore the possible mechanisms.

methodsPancreatic cancer cells expressing IGF1R shRNA were established, and the cell proliferation, colony formation, and chemosensitivity to gemcitabine were examined in vitro. The activation of AKT and NF-κB was detected by Western blot analysis and luciferase assay, respectively. Xenograft mice models were established to evaluate the in vivo anti-tumor effects of IGF1R knockdown.

resultsIGF1R knockdown notably inhibited pancreatic cancer cell proliferation and colony formation, induced apoptosis, and inhibited xenograft tumor growth. Moreover, IGF1R knockdown significantly enhanced chemosensitivity to gemcitabine in pancreatic cancer cells, and this was correlated with the inhibition of PI3K/AKT and NF-κB pathways.

conclusionsIGF1R knockdown suppresses tumor growth and enhances chemosensitivity in pancreatic cancer via the inhibition of PI3K/AKT and NF-κB pathways, and is a promising approach to overcome the chemoresistance of pancreatic cancer.

Indexed as

Drug Resistance, NeoplasmAnimalsAntimetabolites, AntineoplasticCarcinomaCell Line, TumorCell ProliferationDeoxycytidineGemcitabineGene Knockdown TechniquesHumansLentivirusMiceMice, Inbred BALB CMice, NudeNF-kappa BPancreatic NeoplasmsAntimetabolites, AntineoplasticDeoxycytidineGemcitabineNF-kappa BPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptor, IGF Type 1RNA, Small Interfering

Identifiers

PMID23589145
OpenAlexW2022932085

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.