Evidence map›Paper›PMID 28401485›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2017

Silymarin and its active component silibinin act as novel therapeutic alternatives for salivary gland cancer by targeting the ERK1/2-Bim signaling cascade.

Eun-Sun Choi, Sejun Oh, Boonsil Jang, Hyun-Ju Yu, Ji-Ae Shin, Nam-Pyo Cho, In-Hyoung Yang, Dong-Hoon Won, Hye-Jeong Kwon, Seong Doo Hong and 1 more

Abstract read
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 9% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Pooled it
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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

11 authors at 3 institutions in 1 country.

Eun-Sun ChoiDivision of high-risk pathogen research, Korea Centers for Disease Control and Prevention, Osong, 28160, Republic of Korea.
Sejun OhDepartment of Oral Pathology, School of Dentistry and Institute of Biodegradable material, Institute of Oral Bioscience, Chonbuk National University, Brain Korea 21 Project, Jeonju, 54986, Republic of Korea.
Boonsil JangDepartment of Oral Pathology, School of Dentistry and Institute of Biodegradable material, Institute of Oral Bioscience, Chonbuk National University, Brain Korea 21 Project, Jeonju, 54986, Republic of Korea.
Hyun-Ju YuDepartment of Oral Pathology, School of Dentistry and Institute of Biodegradable material, Institute of Oral Bioscience, Chonbuk National University, Brain Korea 21 Project, Jeonju, 54986, Republic of Korea.
Ji-Ae ShinDepartment of Oral Pathology, School of Dentistry and Dental Research Institute, Seoul National University, Seoul, 03080, Republic of Korea.
Nam-Pyo ChoDepartment of Oral Pathology, School of Dentistry and Institute of Biodegradable material, Institute of Oral Bioscience, Chonbuk National University, Brain Korea 21 Project, Jeonju, 54986, Republic of Korea.
In-Hyoung YangDepartment of Oral Pathology, School of Dentistry and Institute of Biodegradable material, Institute of Oral Bioscience, Chonbuk National University, Brain Korea 21 Project, Jeonju, 54986, Republic of Korea.
Dong-Hoon WonDepartment of Oral Pathology, School of Dentistry and Dental Research Institute, Seoul National University, Seoul, 03080, Republic of Korea.
Hye-Jeong KwonDepartment of Oral Pathology, School of Dentistry and Dental Research Institute, Seoul National University, Seoul, 03080, Republic of Korea.
Seong Doo HongDepartment of Oral Pathology, School of Dentistry and Dental Research Institute, Seoul National University, Seoul, 03080, Republic of Korea.
Sung-Dae ChoDepartment of Oral Pathology, School of Dentistry and Dental Research Institute, Seoul National University, Seoul, 03080, Republic of Korea. efiwdsc@snu.ac.kr.
Jeonbuk National University · KRSeoul National University · KRKorea Center for Disease Control and Prevention · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeApproximately 20% of all salivary gland cancer patients who are treated with current treatment modalities will ultimately develop metastases. Its most common form, mucoepidermoid carcinoma (MEC) is a highly aggressive tumor with an overall 5-year survival rate of ~30%. Until now, several chemotherapeutic drugs have been tested for the treatment of salivary gland tumors, but the results have been disappointing and the drugs often cause unwanted side effects. Therefore, several recent studies have focused on the potential of alternative and/or complementary therapeutic options, including the use of silymarin.

methodsThe effects of silymarin and its active component silibinin on salivary gland cancer-derived MC3 and HN22 cells and their underlying molecular mechanisms were examined using trypan blue exclusion, 4'-6-diamidino-2-phenylindole (DAPI) staining, Live/Dead, Annexin V/PI staining, mitochondrial membrane potential (ΔΨm) measurement, quantitative RT-PCR, soft agar colony formation and Western blotting analyses.

resultsWe found that silymarin and silibinin dramatically increased the expression of the pro-apoptotic protein Bim in a concentration- and time-dependent manner and, concomitantly, induced apoptosis in MC3 and HN22 cells. We also found that ERK1/2 signaling inhibition successfully sensitized these cells to the apoptotic effects of silymarin and silibinin, which indicates that the ERK1/2 signaling pathway may act as an upstream regulator that modulates the silymarin/silibinin-induced Bim signaling pathway.

conclusionsTaken together, we conclude that ERK1/2 signaling pathway inhibition by silymarin and silibinin increases the expression of the pro-apoptotic Bcl-2 family member Bim which, subsequently, induces mitochondria-mediated apoptosis in salivary gland cancer-derived cells.

Indexed as

AntioxidantsApoptosisBcl-2-Like Protein 11Cell CycleCell Line, TumorHumansMAP Kinase Signaling SystemSalivary Gland NeoplasmsSilybinSilymarinAntioxidantsBcl-2-Like Protein 11SilybinSilymarinApoptosisERK/Bim signalingSalivary gland tumorSilibininSilymarin

Identifiers

PMID28401485
PMCPMC13001538
OpenAlexW2606634151

What OpenQuestion holds

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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.