Evidence map›Paper›PMID 33649777›Full record

ArticleOncology reports2021

HDAC inhibitors suppress the proliferation, migration and invasiveness of human head and neck squamous cell carcinoma cells via p63‑mediated tight junction molecules and p21‑mediated growth arrest.

Akito Kakiuchi, Takuya Kakuki, Kizuku Ohwada, Makoto Kurose, Atsushi Kondoh, Kazufumi Obata, Kazuaki Nomura, Ryo Miyata, Yakuto Kaneko, Takumi Konno and 4 more

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 7% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

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  15. CDKN1A/p21 in Breast Cancer: Part of the Problem, or Part of the Solution?International journal of molecular sciences · 2023
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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

14 authors at 1 institution in 1 country.

Akito Kakiuchi *Department of Otolaryngology, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo 060‑8556, Japan.
Takuya KakukiDepartment of Otolaryngology, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo 060‑8556, Japan.
Kizuku Ohwada *Department of Otolaryngology, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo 060‑8556, Japan.
Makoto KuroseDepartment of Otolaryngology, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo 060‑8556, Japan.
Atsushi KondohDepartment of Otolaryngology, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo 060‑8556, Japan.
Kazufumi ObataDepartment of Otolaryngology, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo 060‑8556, Japan.
Kazuaki NomuraDepartment of Otolaryngology, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo 060‑8556, Japan.
Ryo MiyataDepartment of Otolaryngology, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo 060‑8556, Japan.
Yakuto KanekoDepartment of Otolaryngology, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo 060‑8556, Japan.
Takumi KonnoDepartment of Cell Science, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo 060‑8556, Japan.
Takayuki KohnoDepartment of Cell Science, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo 060‑8556, Japan.
Tetsuo HimiDepartment of Otolaryngology, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo 060‑8556, Japan.
Ken-Ichi TakanoDepartment of Otolaryngology, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo 060‑8556, Japan.
Takashi KojimaDepartment of Cell Science, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo 060‑8556, Japan.
Sapporo Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In human head and neck squamous cell carcinoma (HNSCC), the invasion and metastatic properties of cancer cells are promoted by junctional adhesion molecule‑A (JAM‑A) and claudin‑1; these are epithelial tight junction molecules regulated by histone deacetylases (HDACs) and transcription factor p63. HDAC expression is reportedly upregulated in HNSCC, and HDAC inhibitors suppress cancer cell proliferation by initiating proliferative arrest or apoptosis. However, little is known of the anti‑cancer mechanisms of HDAC inhibitors in HNSCC. Thus, in the present study, the HNSCC Detroit 562 cell line and primary cultured HNSCC cells were treated with HDAC inhibitors to investigate their effects in HNSCC. Higher expression of p63, HDAC1, JAM‑A and claudin‑1 was observed in HNSCC tissues compared with the adjacent dysplastic regions. In Detroit 562 cells, treatment with trichostatin A (TSA), an inhibitor of HDAC1 and 6, downregulated the expression of p63, JAM‑A and claudin‑1, and upregulated that of acetylated tubulin; conversely, p63 knockdown resulted in the downregulation of JAM‑A and claudin‑1. Collectively, inhibiting HDAC suppressed the migration and invasiveness of cancer cells. In addition, treatment with TSA suppressed cancer cell proliferation via G

Indexed as

AgedApoptosisCell Adhesion MoleculesCell Line, TumorCell MovementCell ProliferationClaudin-1Cyclin-Dependent Kinase Inhibitor p21FemaleG2 Phase Cell Cycle CheckpointsGene Knockdown TechniquesHistone Deacetylase InhibitorsHumansMaleMiddle AgedReceptors, Cell SurfaceCDKN1A protein, humanCell Adhesion MoleculesClaudin-1CLDN1 protein, humanCyclin-Dependent Kinase Inhibitor p21F11R protein, humanHistone Deacetylase InhibitorsReceptors, Cell SurfaceTP63 protein, humanTranscription FactorsTumor Suppressor Proteinsclaudin‑1EGFRHDAC inhibitorshead and neck squamous cell carcinomaJAM‑Ap21p63

Identifiers

PMID33649777
PMCPMC7934225
OpenAlexW3135010555

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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 OpenQuestion graph.