Open Access

Exploring protein profiles and hub genes in ameloblastoma

  • Authors:
    • Sirima Sanguansin
    • Sudaporn Kengkarn
    • Boworn Klongnoi
    • Suthipong Chujan
    • Sittirak Roytrakul
    • Nakarin Kitkumthorn
  • View Affiliations

  • Published online on: February 20, 2024     https://doi.org/10.3892/br.2024.1752
  • Article Number: 64
  • Copyright: © Sanguansin et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Ameloblastoma (AM) is a prominent benign odontogenic tumor characterized by aggressiveness, likely originating from tooth‑generating tissue or the dental follicle (DF). However, proteomic distinctions between AM and DF remain unclear. In the present study, the aim was to identify the distinction between AM and DF in terms of their proteome and to determine the associated hub genes. Shotgun proteomics was used to compare the proteomes of seven fresh‑frozen AM tissues and five DF tissues. Differentially expressed proteins (DEPs) were quantified and subsequently analyzed through Gene Ontology‑based functional analysis, protein‑protein interaction (PPI) analysis and hub gene identification. Among 7,550 DEPs, 520 and 216 were exclusive to AM and DF, respectively. Significant biological pathways included histone H2A monoubiquitination and actin filament‑based movement in AM, as well as pro‑B cell differentiation in DF. According to PPI analysis, the top‑ranked upregulated hub genes were ubiquitin C (UBC), breast cancer gene 1 (BRCA1), lymphocyte cell‑specific protein‑tyrosine kinase (LCK), Janus kinase 1 and ATR serine/threonine kinase, whereas the top‑ranked downregulated hub genes were UBC, protein kinase, DNA‑activated, catalytic subunit (PRKDC), V‑Myc avian myelocytomatosis viral oncogene homolog (MYC), tumor protein P53 and P21 (RAC1) activated kinase 1. When combining upregulated and downregulated genes, UBC exhibited the highest degree and betweenness values, followed by MYC, BRCA1, PRKDC, embryonic lethal, abnormal vision, Drosophila, homolog‑like 1, myosin heavy chain 9, amyloid beta precursor protein, telomeric repeat binding factor 2, LCK and filamin A. In summary, these findings contributed to the knowledge on AM protein profiles, potentially aiding future research regarding AM etiopathogenesis and leading to AM prevention and treatment.
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April-2024
Volume 20 Issue 4

Print ISSN: 2049-9434
Online ISSN:2049-9442

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Spandidos Publications style
Sanguansin S, Kengkarn S, Klongnoi B, Chujan S, Roytrakul S and Kitkumthorn N: Exploring protein profiles and hub genes in ameloblastoma. Biomed Rep 20: 64, 2024.
APA
Sanguansin, S., Kengkarn, S., Klongnoi, B., Chujan, S., Roytrakul, S., & Kitkumthorn, N. (2024). Exploring protein profiles and hub genes in ameloblastoma. Biomedical Reports, 20, 64. https://doi.org/10.3892/br.2024.1752
MLA
Sanguansin, S., Kengkarn, S., Klongnoi, B., Chujan, S., Roytrakul, S., Kitkumthorn, N."Exploring protein profiles and hub genes in ameloblastoma". Biomedical Reports 20.4 (2024): 64.
Chicago
Sanguansin, S., Kengkarn, S., Klongnoi, B., Chujan, S., Roytrakul, S., Kitkumthorn, N."Exploring protein profiles and hub genes in ameloblastoma". Biomedical Reports 20, no. 4 (2024): 64. https://doi.org/10.3892/br.2024.1752