Evidence map›Paper›PMID 39354061›Full record

ArticleScientific reports2024

Ladinin-1 in actin arcs of oral squamous cell carcinoma is involved in cell migration and epithelial phenotype.

Tatsuya Abé, Manabu Yamazaki, Motohiro Nozumi, Satoshi Maruyama, Kaori Takamura, Riuko Ohashi, Yoichi Ajioka, Jun-Ichi Tanuma

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2024. 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
–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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
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

8 authors.

Tatsuya AbéDivision of Oral Pathology, Faculty of Dentistry & Graduate School of Medical and Dental Sciences, Niigata University, 2-5274 Gakkocho-dori, Chuo-ku, Niigata, 951-8514, Japan. abet@dent.niigata-u.ac.jp.
Manabu YamazakiDivision of Oral Pathology, Faculty of Dentistry & Graduate School of Medical and Dental Sciences, Niigata University, 2-5274 Gakkocho-dori, Chuo-ku, Niigata, 951-8514, Japan.
Motohiro NozumiDepartment of Neurochemistry and Molecular Cell Biology, Graduate School of Medicine, Niigata University, Niigata, Japan.
Satoshi MaruyamaOral Pathology Section, Department of Surgical Pathology, Niigata University Hospital, Niigata, Japan.
Kaori TakamuraDivision of Molecular and Diagnostic Pathology, Graduate School of Medical and Dental Sciences, Niigata University, Niigata, Japan.
Riuko OhashiDivision of Molecular and Diagnostic Pathology, Graduate School of Medical and Dental Sciences, Niigata University, Niigata, Japan.
Yoichi AjiokaDivision of Molecular and Diagnostic Pathology, Graduate School of Medical and Dental Sciences, Niigata University, Niigata, Japan.
Jun-Ichi TanumaDivision of Oral Pathology, Faculty of Dentistry & Graduate School of Medical and Dental Sciences, Niigata University, 2-5274 Gakkocho-dori, Chuo-ku, Niigata, 951-8514, Japan.

Funding

Japan Society for the Promotion of Science 18K09550Japan Society for the Promotion of Science 21K09841
6 · The paper itself

Abstract

Histopathologically, oral squamous cell carcinoma (OSCC) consists of well-defined interfaces with adjacent non-cancerous epithelium. Previously, we found that SCC tissues expressed higher levels of specific proteins at this interface. Ladinin-1 (LAD1) is one of the specific molecules that has increased expressions in cancer fronts; however, its function in OSCC is unknown. Therefore, this study aimed to elucidate the function of LAD1 in human OSCC cells. LAD1 was localized on the actin arc at the distal periphery of cell clusters in the OSCC cell lines HSC-2, HSC-3, and HSC-4. When LAD1 was knocked down, cellular migration was repressed in wound scratch assays but was reversed in three-dimensional collagen gel invasion assays. Characteristic LAD1 localization along actin arcs forming the leading edge of migrating cells was diminished with loss of filopodia formation and ruffling in knockdown cells, in which the expression levels of cell motility-related genes-p21-activated kinase 1 (PAK1) and caveolin-1 (CAV1)-were upregulated and downregulated, respectively. LAD1 expression was also associated with the downregulation of vimentin and increased histological differentiation of OSCC. These results suggest that LAD1 is involved in actin dynamics during filopodia and lamellipodia formation, and in maintaining the epithelial phenotype of OSCC cells.

Indexed as

ActinsCarcinoma, Squamous CellCell MovementMouth NeoplasmsCaveolin 1Cell Line, TumorEpithelial CellsExtracellular Matrix ProteinsGene Expression Regulation, NeoplasticHumansp21-Activated KinasesPhenotypeVimentinActinsCAV1 protein, humanCaveolin 1Extracellular Matrix ProteinsLAD1 protein, humanp21-Activated KinasesPAK1 protein, humanVimentinActin arcLadinin-1Squamous cell carcinoma

Identifiers

PMID39354061
PMCPMC11445451

What Socratic 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 Socratic graph.