Evidence map›Paper›PMID 36967712›Full record

ArticleJournal of cellular and molecular medicine2023

Hispolon induces apoptosis in oral squamous cell carcinoma cells through JNK/HO-1 pathway activation.

Wei-En Yang, Yi-Tzu Chen, Chun-Wen Su, Mu-Kuan Chen, Chia-Ming Yeh, Yen-Lin Chen, Meng-Ying Tsai, Shun-Fa Yang, Chiao-Wen Lin

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2023. 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
2.0field-weighted citation impact, top 14% 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, 13 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

9 authors at 2 institutions in 1 country.

Wei-En YangDepartment of Medical Research, Chung Shan Medical University Hospital, Taichung, Taiwan.
Yi-Tzu ChenSchool of Dentistry, Chung Shan Medical University, Taichung, Taiwan.
Chun-Wen SuDepartment of Medical Research, Chung Shan Medical University Hospital, Taichung, Taiwan.
Mu-Kuan ChenDepartment of Otorhinolaryngology-Head and Neck Surgery, Changhua Christian Hospital, Changhua, Taiwan.
Chia-Ming YehDepartment of Medical Research, Chung Shan Medical University Hospital, Taichung, Taiwan.
Yen-Lin ChenSchool of Dentistry, Chung Shan Medical University, Taichung, Taiwan.
Meng-Ying TsaiDepartment of Medical Research, Chung Shan Medical University Hospital, Taichung, Taiwan.
Shun-Fa YangDepartment of Medical Research, Chung Shan Medical University Hospital, Taichung, Taiwan.ORCID 0000-0002-0365-7927
Chiao-Wen LinDepartment of Dentistry, Chung Shan Medical University Hospital, Taichung, Taiwan.
Chung Shan Medical University Hospital · TWChanghua Christian Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oral squamous cell carcinoma (OSCC) has a high recurrence rate and poor prognosis. Hispolon, a polyphenolic compound with antiviral, antioxidant, and anticancer activities, is a potential chemotherapy agent. However, few studies have investigated the anti-cancer mechanism of hispolon in oral cancer. This present study used the cell viability assay, clonogenic assay, fluorescent nuclear staining, and flow cytometry assay to analyse the apoptosis-inducing effects of hispolon in OSCC cells. After hispolon treatment, the apoptotic initiators, cleaved caspase-3, -8, and - 9, were upregulated, whereas the cellular inhibitor of apoptosis protein-1 (cIAP1) was downregulated. Furthermore, a proteome profile analysis using a human apoptosis array revealed the overexpression of heme oxygenase-1 (HO-1) by hispolon, which was determined to be involved in caspase-dependent apoptosis. Moreover, cotreatment with hispolon and mitogen-activated protein kinase (MAPK) inhibitors revealed that hispolon induces apoptosis in OSCC cells through activation of the c-Jun N-terminal kinase (JNK) pathway and not the extracellular signal-regulated kinase (ERK) or p38 pathway. These findings indicate that hispolon may exert an anticancer effect on oral cancer cells by upregulating HO-1 and inducing caspase-dependent apoptosis by activating the JNK pathway.

Indexed as

Carcinoma, Squamous CellHead and Neck NeoplasmsMouth NeoplasmsApoptosisCatecholsCell Line, TumorHeme Oxygenase-1HumansJNK Mitogen-Activated Protein KinasesMAP Kinase Signaling Systemp38 Mitogen-Activated Protein KinasesSquamous Cell Carcinoma of Head and NeckCatecholsHeme Oxygenase-1hispolonJNK Mitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein Kinasesapoptosisheme oxygenase 1hispolonJNK1/2oral squamous cell carcinoma

Identifiers

PMID36967712
PMCPMC10148051
OpenAlexW4361009990

What Socratic 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 Socratic graph.