Evidence map›Paper›PMID 41181426›Full record

ArticleAnnals of medicine and surgery (2012)2025

The role of PD-L1 gene silencing on growth, migration, and apoptosis in oral squamous carcinoma cell line HN-5.

Saeed Nezafati, Aynaz Samadnezhad, Hossein Molapour, Pejman Moradi, Parsa Radesh, Navid Faraji

Abstract read
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Article in Annals of medicine and surgery (2012), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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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

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Saeed NezafatiDepartment of Oral and Maxillofacial Surgery, Faculty of Dentistry, Tabriz University of Medical Sciences, Tabriz, Iran.
Aynaz SamadnezhadDepartment of Prosthodontics, Faculty of Dentistry, Shahid Beheshti University of Medical Science, Tehran, Iran.
Hossein MolapourDepartment of Family Medicine, Faculty of Medicine, Tabriz University of Medical Science, Tabriz, Iran.
Pejman MoradiDepartment of Prosthodontics, Faculty of Dentistry, Shahid Beheshti University of Medical Science, Tehran, Iran.
Parsa RadeshDepartment of Prosthodontics, Faculty of Dentistry, Shahid Beheshti University of Medical Science, Tehran, Iran.
Navid FarajiDepartment of Medical-Surgical Nursing School of Nursing and Midwifery, Urmia University of Medical Sciences, Urmia, Iran.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction and importance: Oral cavity squamous cell carcinoma (OCSCC) presents a major risk to worldwide health. Its advancement is often associated with elevated concentrations of programmed cell death protein 1 (PD-1) and programmed death-ligand 1 (PD-L1), which create an immunosuppressive environment, hindering the capability of the immune system to fight tumors. By targeting PD-L1 through gene silencing, there is potential to enhance immune responses against OCSCC and inhibit tumor growth. This study explores the impact of PD-L1 suppression on the HN-5 OCSCC cell line, with a focus on cell growth, apoptosis, cell cycle progression, and migration. Methods: We evaluated the effects of PD-L1 gene silencing on the proliferation and survival of HN-5 cells using the MTT assay. Flow cytometry was utilized to investigate apoptosis induction and cell cycle arrest in cells with reduced PD-L1 expression. A wound healing test was performed to assess the impact of PD-L1 silencing on the movement of OCSCC cells. Additionally, quantitative reverse transcription polymerase chain reaction (qRT-PCR) was conducted to analyze the expression of genes related to apoptosis. Results: The use of PD-L1 small interfering RNA (siRNA) effectively lowered PD-L1 mRNA levels in HN-5 cells, resulting in reduced cell proliferation. Knockdown of PD-L1 leading to enhanced apoptosis and a halt in the cell cycle during the G1 phase. Further analysis indicated that silencing PD-L1 upregulated Caspase-9 (CAS-9), cellular Myelocytomatosis oncogene (c-Myc), and Bcl-2-associated X protein (Bax), while lowering the levels of B-Cell Lymphoma 2 (BCL-2). The migratory ability of cells treated with PD-L1 siRNA was significantly diminished compared to control cells. Conclusion: In summary, our findings suggest that knocking down PD-L1 in the HN-5 cell line could serve as a promising approach for treating oral cavity squamous cell carcinoma (OCSCC). This highlights how crucial the PD-1/PD-L1 pathway is in the formation and progression of these types of tumors.

Indexed as

immune checkpointoral cavityPD-L1siRNAsquamous cell carcinoma

Identifiers

PMID41181426
PMCPMC12577905

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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.