Evidence map›Paper›PMID 36737832›Full record

ArticleJournal of experimental & clinical cancer research : CR2023

MiR-455-5p suppresses PDZK1IP1 to promote the motility of oral squamous cell carcinoma and accelerate clinical cancer invasion by regulating partial epithelial-to-mesenchymal transition.

Sheng-Yen Hsiao, Shang-Mei Weng, Jenn-Ren Hsiao, Yi-Ying Wu, Jia-En Wu, Chia-Hao Tung, Wan-Lin Shen, Shu-Fang Sun, Wen-Tsung Huang, Cheng-Yao Lin and 4 more

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.7field-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

15 citing papers in PubMed, 24 citations in OpenAlex.

  1. 4-1BBCell reports. Medicine · 2025
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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 4 institutions in 1 country.

Sheng-Yen HsiaoInstitute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Shang-Mei WengDivision of Hematology-Oncology, Department of Internal Medicine, Chi Mei Medical Center, Liouying, Tainan, Taiwan.
Jenn-Ren HsiaoDepartment of Otolaryngology, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Yi-Ying WuClinical Medicine Research Center, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Jia-En WuInstitute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Chia-Hao TungInstitute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Wan-Lin ShenDepartment of Pathology, Chi Mei Medical Center, Liouying, Tainan, Taiwan.
Shu-Fang SunDivision of Hematology-Oncology, Department of Internal Medicine, Chi Mei Medical Center, Liouying, Tainan, Taiwan.
Wen-Tsung HuangDivision of Hematology-Oncology, Department of Internal Medicine, Chi Mei Medical Center, Liouying, Tainan, Taiwan.
Cheng-Yao LinDivision of Hematology-Oncology, Department of Internal Medicine, Chi Mei Medical Center, Liouying, Tainan, Taiwan.
Shang-Hung ChenNational Institute of Cancer Research, National Health Research Institutes, Tainan, Taiwan.
Tse-Ming HongInstitute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan. tmhong@ncku.edu.tw.
Yuh-Ling ChenInstitute of Oral Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan. yuhling@ncku.edu.tw.ORCID http://orcid.org/0000-0001-7760-5954
Jang-Yang ChangInstitute of Biotechnology and Pharmaceutical Research, National Health Research Institutes, Miaoli, Taiwan. jychang@nhri.edu.tw.
Chi Mei Medical Center · TWNational Cheng Kung University · TWNational Cheng Kung University Hospital · TWNational Health Research Institutes · TW

Funding

Chi Mei Medical Center CLFHR11023Ministry of Science and Technology MOST 109-2314-B-384-009Ministry of Science and Technology MOST 111-2314-B-384 -005Ministry of Science and Technology, Taiwan MOST 110-2314-B-006-073-MY3
6 · The paper itself

Abstract

backgroundLymph node and distant metastasis contribute to poor outcomes in patients with oral squamous cell carcinoma (OSCC). The mechanisms regulating cancer migration and invasion play a key role in OSCC.

methodsWe determined migration and invasion ability of OSCC by wound-healing assay, two-chamber transwell invasion assay and cell mobility tracking and evaluated tumor metastasis in vivo. Western blot (WB), qRT-PCR, RNA-seq, dual-luciferase reporter assays and nuclear/cytoplasmic fractionation were performed to investigate the potential mechanism. Immunohistochimical (IHC) staining determined vimentin and PDZK1IP1 expression in OSCC tissues. RESULTS AND

conclusionIn this study, we determined that miR-455-5p was associated with lymph node metastasis and clinical invasion, leading to poor outcomes in patients with OSCC. MiR-455-5p promoted oral cancer cell migration and invasion and induced epithelial-to-mesenchymal transition (EMT). We also identified a new biomarker, PDZK1IP1 (MAP17), that was targeted by miR-455-5p. PDZK1IP1 knockdown led to migration, metastasis, EMT, and increased transforming growth factor-β signaling in OSCC. In addition, miR-455-5p overexpression and PDZK1IP1 inhibition promoted collective OSCC cell migration. According to data from the Cancer Genome Atlas database and the NCKU-OrCA-40TN data set, miR-455-5p and PDZK1IP1 are positively and negatively correlated, respectively, with partial EMT score. High miR-455-5p expression was associated with high vimentin levels and low MAP17 H-scores. The patients with low MAP17 expression had higher rates of disease recurrence than did patients with high MAP17 expression, especially for patients with clinical invasion risk factors and low MAP17 expression. These results suggest that miR-455-5p suppresses PDZK1IP1 expression and mediates OSCC progression. MiR-455-5p and PDZK1IP1 may therefore serve as key biomarkers and be involved in regulating partial EMT in OSCC cells. PDZK1IP1 expression may also serve as an independent factor that impacts outcomes in patients with clinical risk factors for recurrence.

Indexed as

Carcinoma, Squamous CellHead and Neck NeoplasmsMicroRNAsMouth NeoplasmsBiomarkersCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansMembrane ProteinsNeoplasm Recurrence, LocalSquamous Cell Carcinoma of Head and NeckVimentinBiomarkersMembrane ProteinsMicroRNAsMIRN455 microRNA, humanPDZK1IP1 protein, humanVimentinmiR-455-5pPartial epithelial-to-mesenchymal transitionPDZK1IP1

Identifiers

PMID36737832
PMCPMC9896797
OpenAlexW4319083909

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.