Evidence map›Paper›PMID 26911335›Full record

ArticleBMC nephrology2016

Resveratrol attenuates constitutive STAT3 and STAT5 activation through induction of PTPε and SHP-2 tyrosine phosphatases and potentiates sorafenib-induced apoptosis in renal cell carcinoma.

Chulwon Kim, Sang Hyun Baek, Jae-Young Um, Bum Sang Shim, Kwang Seok Ahn

Open access · goldAbstract read
In one paragraph

Article in BMC nephrology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.9field-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

34 citing papers in PubMed, 60 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

5 authors at 1 institution in 1 country.

Chulwon KimDepartment of Science in Korean Medicine, College of Korean Medicine, Kyung Hee University, 24 Kyungheedae-ro, Dongdaemungu, Seoul, 130-701, Republic of Korea. sunny10526@nate.com.
Sang Hyun BaekDepartment of Science in Korean Medicine, College of Korean Medicine, Kyung Hee University, 24 Kyungheedae-ro, Dongdaemungu, Seoul, 130-701, Republic of Korea. blithe100@naver.com.
Jae-Young UmDepartment of Science in Korean Medicine, College of Korean Medicine, Kyung Hee University, 24 Kyungheedae-ro, Dongdaemungu, Seoul, 130-701, Republic of Korea. jyum@khu.ac.kr.
Bum Sang ShimDepartment of Science in Korean Medicine, College of Korean Medicine, Kyung Hee University, 24 Kyungheedae-ro, Dongdaemungu, Seoul, 130-701, Republic of Korea. eshimbs@khu.ac.kr.
Kwang Seok AhnDepartment of Science in Korean Medicine, College of Korean Medicine, Kyung Hee University, 24 Kyungheedae-ro, Dongdaemungu, Seoul, 130-701, Republic of Korea. ksahn@khu.ac.kr.
Kyung Hee University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSignal transducers and activators of transcription (STAT) proteins are critical transcription factor that are aberrantly activated in various types of malignancies, including renal cell carcinoma (RCC).

methodsWe investigated the effect of resveratrol (RES), an edible polyphenol phytoalexin on STAT3 and STAT5 activation cascade in both Caki-1 and 786-O RCC cell lines.

resultsWe found that RES suppressed both constitutive STAT3 (tyrosine residue 705 and serine residue 727) and STAT5 (tyrosine residue 694 and 699) activation, which correlated with the suppression of the upstream kinases (JAK1, JAK2, and c-Src) in RCC. Also, RES abrogated DNA binding capacity and nuclear translocation of these two transcription factors. RES-induced an increased expression of PTPε and SHP-2 and the deletion of these two genes by small interfering RNA abolished the ability of RES to inhibit STAT3 activation, suggesting the critical role of both PTPε and SHP-2 in its possible mechanism of action. Moreover, RES induced S phase cell cycle arrest, caused induction of apoptosis, loss of mitochondrial membrane potential, and suppressed colony formation in RCC. We also found that RES downregulated the expression of STAT3/5-regulated antiapoptotic, proliferative, and metastatic gene products; and this correlated with induction of caspase-3 activation and anti-invasive activity. Beside, RES potentiated sorafenib induced inhibitory effect on constitutive STAT3 and STAT5 phosphorylation, apoptotic effects in 786-O cells, and this correlated with down-regulation of various oncogenic gene products.

conclusionOverall, our results suggest that RES is a blocker of both STAT3 and STAT5 activation and thus may exert potential growth inhibitory effects against RCC cells.

Indexed as

Antineoplastic AgentsAntineoplastic Agents, PhytogenicApoptosisCarcinoma, Renal CellCell Line, TumorCell MovementCell SurvivalHumansKidney NeoplasmsMembrane Potential, MitochondrialNiacinamidePhenylurea CompoundsProtein Tyrosine Phosphatase, Non-Receptor Type 11Receptor-Like Protein Tyrosine Phosphatases, Class 4ResveratrolSignal TransductionAntineoplastic AgentsAntineoplastic Agents, PhytogenicNiacinamidePhenylurea CompoundsProtein Tyrosine Phosphatase, Non-Receptor Type 11PTPN11 protein, humanReceptor-Like Protein Tyrosine Phosphatases, Class 4ResveratrolSorafenibSTAT3 protein, humanSTAT3 Transcription FactorSTAT5 Transcription FactorStilbenes

Identifiers

PMID26911335
PMCPMC4766620
OpenAlexW2278151798

What OpenQuestion holds

Textmetadata
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.