Evidence map›Paper›PMID 27847436›Full record

ArticleThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology2016

The p90rsk-mediated signaling of ethanol-induced cell proliferation in HepG2 cell line.

Han Sang Kim, Su-Jin Kim, Jinhyung Bae, Yiyi Wang, Sun Young Park, Young Sil Min, Hyun Dong Je, Uy Dong Sohn

Open access · diamondAbstract read
In one paragraph

Article in The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

9 citing papers in PubMed, 17 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

8 authors at 1 institution in 1 country.

Han Sang KimDepartment of Pharmacology, College of Pharmacy, Chung-Ang University, Seoul 06974, Korea.
Su-Jin KimDepartment of Pharmacology, College of Pharmacy, Chung-Ang University, Seoul 06974, Korea.
Jinhyung BaeDepartment of Pharmacology, College of Pharmacy, Chung-Ang University, Seoul 06974, Korea.
Yiyi WangDepartment of Pharmacology, College of Pharmacy, Chung-Ang University, Seoul 06974, Korea.
Sun Young ParkDepartment of Pharmacology, College of Pharmacy, Chung-Ang University, Seoul 06974, Korea.
Young Sil MinDepartment of Medicinal Plant Science, College of Science and Engineering, Jungwon University, Chungbuk 28024, Korea.
Hyun Dong JeDepartment of Pharmacology, College of Pharmacy, Catholic University of Daegu, Daegu 38430, Korea.
Uy Dong SohnDepartment of Pharmacology, College of Pharmacy, Chung-Ang University, Seoul 06974, Korea.
Chung-Ang University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ribosomal S6 kinase is a family of serine/threonine protein kinases involved in the regulation of cell viability. There are two subfamilies of ribosomal s6 kinase, (p90rsk, p70rsk). Especially, p90rsk is known to be an important downstream kinase of p44/42 MAPK. We investigated the role of p90rsk on ethanol-induced cell proliferation of HepG2 cells. HepG2 cells were treated with 10~50 mM of ethanol with or without ERK and p90rsk inhibitors. Cell viability was measured by MTT assay. The expression of pERK1, NHE1 was measured by Western blots. The phosphorylation of p90rsk was measured by ELISA kits. The expression of Bcl-2 was measured by qRT-PCR. When the cells were treated with 10~30 mM of ethanol for 24 hour, it showed significant increase in cell viability versus control group. Besides, 10~30 mM of ethanol induced increased expression of pERK1, p-p90rsk, NHE1 and Bcl-2. Moreover treatment of p90rsk inhibitor attenuated the ethanol-induced increase in cell viability and NHE1 and Bcl-2 expression. In summary, these results suggest that p90rsk, a downstream kinase of ERK, plays a stimulatory role on ethanol-induced hepatocellular carcinoma progression by activating anti-apoptotic factor Bcl-2 and NHE1 known to regulate cell survival.

Indexed as

Bcl-2EthanolHepatocellular carcinomaNHE1p90rsk

Identifiers

PMID27847436
PMCPMC5106393
OpenAlexW2553630505

What OpenQuestion holds

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LicenceCC BY-NC
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.