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2023, vol. 151, br. 1-2, str. 15-20
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Ekspresija gena STAT3 kod ameloblastoma i odontogenih keratocista
STAT3 gene expression in ameloblastomas and odontogenic keratocysts
aFederalni univerzitet Baije, Stomatološki fakultet, Laboratorija za hiruršku patologiju, Salvador, Brazil bFederalni univerzitet Baije, Program stomatologije i zdravlja, Salvador, Brazil cFederalni univerzitet Baije, Odeljenje za biomorfologiju, Salvador, Brazil dJužni univerzitet u Baiji, Odeljenje za oralnu i maksilofacijalnu hirurgiju, Žekije, Brazil eUniverzitet u Sao Paulu, Odeljenje za oralnu i maksilofacijalnu patologiju, Sao Paulo, Brazil fDržavni univerzitet u Feiri de Santani, Zdravstveni program, Feira de Santana, Brazil gFederalni univerzitet Baije, Stomatološki fakultet, Laboratorija za hiruršku patologiju, Salvador, Brazil + Federalni univerzitet Baije, Program stomatologije i zdravlja, Salvador, Brazil
e-adresa: andradedandara@gmail.com
Projekat: This study was funded by the National Council for Scientific and Technological Development (CNPq)
This study was funded by the Coordination for the Improvement of Higher Education Personnel (CAPES)
Sažetak
Uvod/Cilj STAT3 (pretvarači signala i aktivatori transkripcije) uključen je u različite fiziološke procese, uključujući proliferaciju i preživljavanje ćelija. Visoka ekspresija ovog proteina se primećuje kod različitih vrsta raka. Ova studija je imala za cilj da istraži ekspresiju gena i proteina STAT3 u seriji odontogenih cista i tumora kako bi pružila više informacija o njihovom biološkom profilu. Metode Ekspresija gena STAT3 na mRNK je kvantifikovana kvantitativnom lančanom reakcijom polimeraze u realnom vremenu (RT-kPCR) u 23 odontogene keratociste (OKC) i sedam ameloblastoma (AM) i upoređena sa neneoplastičnom oralnom sluznicom. Takođe smo procenili ekspresiju gena STAT3 na nivoima proteina, koristeći imunohistohemiju, u 43 OKC i 47 AM. Rezultati STAT3 transkripti su pronađeni u 96,6% proučavanih tumora; međutim, GEN je smanjen u OKC i AM u poređenju sa neneoplastičnom oralnom sluzokožom. Ekspresija STAT3 gena na nivou mRNK bila je veća kod sporadičnog OKC nego kod sindromskog STAT3 (p = 0,04). Nije bilo razlike u ekspresiji STAT3 gena na nivou mRNA između OKC i AMs (p = 0,88). Imunobojenje STAT3 nije otkrilo značajnu razliku između sporadičnog i sindroma OKC (p > 0,05), niti između konvencionalnih i unicističnih AM (p > 0,05). Ameloblastomi su pokazali značajno veće STAT3 imunobojenje od OKC (p = 0,03). Kod OKC i AM, STAT3 imunobojenje je bilo pretežno citoplazmatsko i nije primećena razlika u ćelijskoj lokalizaciji STAT3 između ovih lezija (p = 0,58). Zaključak Naši nalazi su pokazali nisku ekspresiju gena STAT3 u OKC i AMs u odnosu na neneoplastičnu oralnu sluzokožu. Međutim, primećeno je veće STAT3 imunobojenje kod AM u poređenju sa OKC.
Abstract
Introduction/Objective STAT3 (signal transducers and activators of transcription) is involved in different physiological processes, including cell proliferation and survival. High expression of this protein is observed in various types of cancer. This study aimed to investigate the gene and protein expression of STAT3 in a series of odontogenic cysts and tumors to provide more information about their biological profile. Methods The STAT3 gene expression at mRNA was quantified by real-time quantitative polymerase chain reaction (RT-qPCR) in 23 odontogenic keratocysts (OKCs) and seven ameloblastomas (AMs), and compared to the non-neoplastic oral mucosa. We also assessed the expression of STAT3 gene at protein levels, using immunohistochemistry, in 43 OKCs and 47 AMs. Results STAT3 transcripts were found in 96.6% of the tumors studied; however, the gene was downregulated in OKC and AM compared to the non-neoplastic oral mucosa. The STAT3 gene expression at mRNA level was higher in sporadic OKC than in syndromic OKC (p = 0.04). There was no difference in STAT3 gene expression at mRNA level between OKCs and AMs (p = 0.88). Immunostaining of STAT3 revealed no significant difference between sporadic and syndrome OKC (p > 0.05), nor between conventional and unicystic AMs (p > 0.05). Ameloblastomas exhibited significantly higher STAT3 immunostaining than OKCs (p = 0.03). In OKC and AM, STAT3 immunostaining was predominantly cytoplasmic and no difference in the cellular localization of STAT3 was observed between these lesions (p = 0.58). Conclusion Our findings showed low expression of STAT3 gene in OKCs and AMs in relation to non-neoplastic oral mucosa. However, higher STAT3 immunostaining was observed in AMs compared to OKCs.
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