Evidence map›Paper›PMID 37144504›Full record

ArticleOncology reports2023

Anti‑tumor properties of FoxO1 in YD‑9 oral squamous cell carcinoma cells.

Yu Gyung Kim, Chaeeun Seong, Kyoung-Ah Cho, Sang Min Lee, Tae-Jun Kim, Hyeon Ji Kim, Jin-Hwa Cho, Won Jung, Sungil Jang, Jae-Cheon Shin and 3 more

Abstract read
In one paragraph

Article in Oncology reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

13 authors.

Yu Gyung Kim *Department of Pharmacology, School of Dentistry, Kyungpook National University, Daegu 41940, Republic of Korea.
Chaeeun Seong *Department of Pharmacology, School of Dentistry, Kyungpook National University, Daegu 41940, Republic of Korea.
Kyoung-Ah Cho *Department of Oral Medicine, School of Dentistry, Kyungpook National University, Daegu 41940, Republic of Korea.
Sang Min LeeDepartment of Pharmacology, School of Dentistry, Kyungpook National University, Daegu 41940, Republic of Korea.
Tae-Jun KimDepartment of Pharmacology, School of Dentistry, Kyungpook National University, Daegu 41940, Republic of Korea.
Hyeon Ji KimDepartment of Pharmacology, School of Dentistry, Kyungpook National University, Daegu 41940, Republic of Korea.
Jin-Hwa ChoDepartment of Pharmacology, School of Dentistry, Kyungpook National University, Daegu 41940, Republic of Korea.
Won JungDepartment of Oral Medicine, Institute of Oral Bioscience, School of Dentistry, Jeonbuk National University, Jeonju 54896, Republic of Korea.
Sungil JangDepartment of Oral Biochemistry, Institute of Oral Bioscience, School of Dentistry, Jeonbuk National University, Jeonju 54896, Republic of Korea.
Jae-Cheon ShinAdvanced Bio‑Convergence Center, Pohang Technopark, Pohang 37668, Republic of Korea.
Kyung-Ha LeeDepartment of Molecular Biology, Pusan National University, Busan 46241, Republic of Korea.
Jin-Seok ByunDepartment of Oral Medicine, School of Dentistry, Kyungpook National University, Daegu 41940, Republic of Korea.
Do-Yeon KimDepartment of Pharmacology, School of Dentistry, Kyungpook National University, Daegu 41940, Republic of Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oral squamous cell carcinoma (OSCC) is a tumor with a poor prognosis and a high recurrence rate. Despite its high annual incidence worldwide, appropriate therapeutic strategies have not yet been developed. Consequently, the 5‑year survival rate for OSCC is low when advanced stages or recurrence is diagnosed. Forkhead transcriptional factor O1 (FoxO1) is a key mediator for maintaining cellular homeostasis. FoxO1 can function as a tumor suppressor as well as an oncogene depending on the cancer type. Therefore, the precise molecular functions of FoxO1 need to be validated, considering intracellular factors and the extracellular environment. To the best of our knowledge, however, the roles of FoxO1 in OSCC have not yet been defined. The present study examined FoxO1 levels under pathological conditions (oral lichen planus and oral cancer) and selected an appropriate OSCC cell line (YD‑9). Crispr/Cas9 was used to generate FoxO1‑deficient YD‑9 cells in which the protein levels of phospho ERK and phospho STAT3 were upregulated, promoting cancer proliferation and migration. In addition, FoxO1 reduction increased the levels of the cell proliferation markers phospho H3 (Ser10) and PCNA. FoxO1 loss significantly reduced cellular ROS levels and apoptosis in YD‑9 cells. Collectively, the present study demonstrated that FoxO1 exerted an anti‑tumor effect by suppressing proliferation and migration/invasion but promoting oxidative stress‑linked cell death in YD‑9 OSCC cells.

Indexed as

Carcinoma, Squamous CellHead and Neck NeoplasmsMouth NeoplasmsCell Line, TumorCell MovementCell ProliferationForkhead Box Protein O1HumansSquamous Cell Carcinoma of Head and NeckForkhead Box Protein O1FOXO1 protein, humanforkhead transcriptional factor O1oral squamous cell carcinomaproliferationreactive oxygen species

Identifiers

PMID37144504
PMCPMC10173376

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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.