Evidence map›Paper›PMID 34391437›Full record

ArticleCancer cell international2021

Molecular mechanism underlying the apoptotic modulation by ethanol extract of Pseudolarix kaempferi in mucoepidermoid carcinoma of the salivary glands.

Su-Jung Choi, Chi-Hyun Ahn, Kyoung-Ok Hong, Ji-Hoon Kim, Seong-Doo Hong, Ji-Ae Shin, Sung-Dae Cho

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.5field-weighted citation impact, top 38% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
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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

7 authors at 2 institutions in 2 countries.

Su-Jung ChoiDepartment of Oral Pathology, School of Dentistry and Dental Research Institute, Seoul National University, 03080, Seoul, Republic of Korea.
Chi-Hyun AhnDepartment of Oral Pathology, School of Dentistry and Dental Research Institute, Seoul National University, 03080, Seoul, Republic of Korea.
Kyoung-Ok HongDepartment of Oral Pathology, School of Dentistry and Dental Research Institute, Seoul National University, 03080, Seoul, Republic of Korea.
Ji-Hoon KimDepartment of Oral Pathology, School of Dentistry and Dental Research Institute, Seoul National University, 03080, Seoul, Republic of Korea.
Seong-Doo HongDepartment of Oral Pathology, School of Dentistry and Dental Research Institute, Seoul National University, 03080, Seoul, Republic of Korea.
Ji-Ae ShinDepartment of Oral Pathology, School of Dentistry and Dental Research Institute, Seoul National University, 03080, Seoul, Republic of Korea. sky21sm@snu.ac.kr.ORCID http://orcid.org/0000-0002-5407-2611
Sung-Dae ChoDepartment of Oral Pathology, School of Dentistry and Dental Research Institute, Seoul National University, 03080, Seoul, Republic of Korea. efiwdsc@snu.ac.kr.
Seoul National University · KRInstitut Pasteur Korea · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPseudolarix kaempferi is a traditional Chinese natural product that possesses the potential cytotoxic effects against cancer. However, the precise molecular mechanism underlying its cytotoxic effects has not yet been completely elucidated. Here, we clarify the mechanism via which the ethanol extract of P. kaempferi (EEPK) leads to cytotoxicity mediated by apoptosis in mucoepidermoid carcinoma (MEC) originating from the salivary glands.

methodsWe investigated the mechanism underlying the anticancer efficacy of EEPK in human MEC in vitro by assessing mitochondrial dysfunction, mRNA levels, and morphological changes in apoptotic cell nuclei as well as by using a cytotoxicity assay, flow cytometric analysis, and western blotting.

resultsEEPK inhibited the growth of two human MEC cells and stimulated the induction of caspase-mediated apoptosis that was accompanied by mitochondrial membrane depolarization. Compared with the vehicle control groups, EEPK decreased myeloid cell leukemia-1 (Mcl-1) expression in both cells whereas it significantly decreased B cell lymphoma-2 (Bcl-2) expression in MC3 cells only. The EEPK-induced altered Mcl-1 expression was caused by translational inhibition and proteasomal degradation. Additionally, EEPK significantly increased p-Bcl-2 (Ser

conclusionsThis study revealed that EEPK-induced alterations of Mcl-1 inhibition and JNK/Bcl-2 phosphorylation cause apoptosis and provided basic preclinical data for future clinical trials regarding therapy for patients with MEC.

Indexed as

ApoptosisBcl-2JNK signaling pathwayMcl-1Mucoepidermoid carcinomaPhosphorylationPseudolarix kaempferi

Identifiers

PMID34391437
PMCPMC8364062
OpenAlexW3194920117

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.