Evidence map›Paper›PMID 30838710›Full record

ArticleCell proliferation2019

Insulin promotes invasion and migration of KRAS

Guangfu Wang, Lingdi Yin, Yunpeng Peng, Yong Gao, Hao Gao, Jingjing Zhang, Nan Lv, Yi Miao, Zipeng Lu

Open access · goldAbstract read
In one paragraph

Article in Cell proliferation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

21 citing papers in PubMed, 26 citations in OpenAlex.

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  18. Current mechanisms in obesity and tumor progression.Current opinion in clinical nutrition and metabolic care · 2020
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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 1 institution in 1 country.

Guangfu WangPancreas Center, First Affiliated Hospital of Nanjing Medical University, Nanjing, China.ORCID http://orcid.org/0000-0003-4065-1054
Lingdi YinPancreas Center, First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Yunpeng PengPancreas Center, First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Yong GaoPancreas Center, First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Hao GaoPancreas Center, First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Jingjing ZhangPancreas Center, First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Nan LvPancreas Center, First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Yi MiaoPancreas Center, First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Zipeng LuPancreas Center, First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Jiangsu Province Hospital · CN

Funding

Innovation Capability Development Project of Jiangsu Province BM2015004National Natural Science Foundation of China 81672449Science, Technology and Education, Jiangsu Provincial Medical Outstanding Talent JCRCA2016009
6 · The paper itself

Abstract

objectivesHyperinsulinemia is a risk factor for pancreatic cancer, but the function of insulin in carcinogenesis is unclear, so this study aimed to elucidate the carcinogenic effects of insulin and the synergistic effect with the KRAS mutation in the early stage of pancreatic cancer. MATERIALS AND

methodsA pair of immortalized human pancreatic duct-derived cells, hTERT-HPNE E6/E7/st (HPNE) and its oncogenic KRAS

resultsThe migration and invasion ability of HPNE cells was increased after the introduction of the mutated KRAS gene, together with an increased expression of MMP-2. These effects were further enhanced by the simultaneous administration of insulin. The use of MMP-2 siRNA confirmed that MMP-2 was involved in the regulation of cell invasion. Furthermore, there was a concentration- and time-dependent increase in gelatinase activity after insulin treatment, which could be reversed by an insulin receptor tyrosine kinase inhibitor (HNMPA-(AM)

conclusionsTaken together, these results suggest that insulin induced migration and invasion in HPNE and HPNE-mut-KRAS through PI3K/AKT and ERK1/2 activation, with MMP-2 gelatinolytic activity playing a vital role in this process. These findings may provide a new therapeutic target for preventing carcinogenesis and the evolution of pancreatic cancer with a background of hyperinsulinemia.

Indexed as

Antigens, CDCarcinogenesisCell LineCell Line, TumorCell MovementCell ProliferationHumansInsulinMAP Kinase Signaling SystemMatrix Metalloproteinase 2Models, BiologicalNeoplasm InvasivenessPancreatic DuctsPancreatic NeoplasmsPhosphatidylinositol 3-KinasesPoint MutationAntigens, CDINSR protein, humanInsulinKRAS protein, humanMatrix Metalloproteinase 2MMP2 protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins p21(ras)Receptor, InsulinRNA, Small Interferinggelatinolytic activityinsulinmigration and invasionMMP-2

Identifiers

PMID30838710
PMCPMC6536446
OpenAlexW2921677415

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.