Evidence map›Paper›PMID 34769290›Full record

ArticleInternational journal of molecular sciences2021

FLLL32 Triggers Caspase-Mediated Apoptotic Cell Death in Human Oral Cancer Cells by Regulating the p38 Pathway.

Chun-Wen Su, Chun-Yi Chuang, Yi-Tzu Chen, Wei-En Yang, Yi-Ping Pan, Chiao-Wen Lin, Shun-Fa Yang

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

18 citing papers in PubMed, 20 citations in OpenAlex.

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  14. Hemoxygenase-1 Promotes Head and Neck Cancer Cell Viability.Antioxidants (Basel, Switzerland) · 2022
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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 1 institution in 1 country.

Chun-Wen SuInstitute of Medicine, Chung Shan Medical University, Taichung 402, Taiwan.
Chun-Yi ChuangSchool of Medicine, Chung Shan Medical University, Taichung 402, Taiwan.
Yi-Tzu ChenSchool of Dentistry, Chung Shan Medical University, Taichung 402, Taiwan.ORCID 0000-0002-6022-7085
Wei-En YangInstitute of Medicine, Chung Shan Medical University, Taichung 402, Taiwan.
Yi-Ping PanInstitute of Medicine, Chung Shan Medical University, Taichung 402, Taiwan.
Chiao-Wen LinInstitute of Oral Sciences, Chung Shan Medical University, Taichung 402, Taiwan.
Shun-Fa YangInstitute of Medicine, Chung Shan Medical University, Taichung 402, Taiwan.ORCID 0000-0002-0365-7927
Chung Shan Medical University Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oral cancer is the most common oral malignant tumor in Taiwan. Although there exist several methods for treatment, oral cancer still has a poor prognosis and high recurrence. FLLL32, a synthetic analog of curcumin with antitumor activity, is currently known to induce melanoma apoptosis and inhibit tumor growth in various cancers. However, few studies have examined the mechanisms of FLLL32 in oral cancer. In this study, we explore whether FLLL32 induces apoptosis in oral cancer. We determined that FLLL32 can inhibit the cell viability of oral cancer. Next, we analyzed the effect of FLLL32 on the cell cycle of oral cancer cells and observed that the proportion of cells in the G2/M phase was increased. Additionally, annexin-V/PI double staining revealed that FLLL32 induced apoptosis in oral cancer cells. Data from the Human Apoptosis Array revealed that FLLL32 increases the expression of cleaved caspase-3 and heme oxygenase-1 (HO-1). FLLL32 activates proteins such as caspase-8, caspase-9, caspase-3, PARP, and mitogen-activated protein kinases (MAPKs) in apoptosis-related molecular mechanisms. Moreover, by using MAPK inhibitors, we suggest that FLLL32 induces the apoptosis of oral cancer cells through the p38 MAPK signaling pathway. In conclusion, our findings suggest that FLLL32 is a potential therapeutic agent for oral cancer by inducing caspase-dependent apoptosis and HO-1 activation through the p38 pathway. We believe that the activation of HO-1 and the p38 pathway by FLLL32 represent potential targets for further research in oral cancer.

Indexed as

Carcinoma, Squamous CellCaspase 3Cell CycleCell Line, TumorCell ProliferationCell SurvivalCurcuminGene Expression Regulation, NeoplasticHeme Oxygenase-1HumansMAP Kinase Signaling SystemMouth NeoplasmsCASP3 protein, humanCaspase 3CurcuminFLLL 32Heme Oxygenase-1HMOX1 protein, humanapoptosisFLLL32HO-1oral cancerp38

Identifiers

PMID34769290
PMCPMC8584525
OpenAlexW3209033247

What Socratic holds

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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.