Expression of cyclooxygenase-2, peroxiredoxin I, peroxiredoxin 6 and nuclear factor-κB in oral squamous cell carcinoma

Abstract

Abstract. Tumor development and progression are multistep processes that involve local tumor growth and invasion, followed by metastasis. The aggressiveness of the tumor is the major determinant of the mortality of oral cancer patients. The present study investigates whether the expression levels of cyclooxygenase-2 (COX-2), nuclear factor-κB (NF-κB), peroxiredoxin 1 (PRDX1) and PRDX6 are associated with the development, proliferation, differentiation and recurrence of oral squamous cell carcinoma (OSCC). The mRNA expression levels of COX-2, NF-κB, PRDX1 and PRDX6 were examined in 50 OSCC specimens and 19 normal oral mucosae by quantitative polymerase chain reaction (qPCR). qPCR analysis showed that the mRNA levels of COX-2 in OSCC were significantly higher than those in the normal oral mucosae (P=0.021). The expression levels of PRDX1 in high-stage tumors (T3 and T4) were significantly elevated compared with those in low-stage tumors (T1) (P=0.047). Additionally, the expression levels of NF-κB in the high-grade tumor were significantly elevated compared with those in the low-grade tumors (P=0.030). Overall, it was indicated that the expression of COX-2 is strongly associated with the development of OSCC. Moreover, the enhanced expression of PRDX1 and NF-κB may function in the progression of OSCC, which serves as a useful marker for prognosis in patients with oral cancer.

Nrf2-peroxiredoxin I axis in polymorphous adenocarcinoma is associated with low matrix metalloproteinase 2 level

“…1g), while OSCC, used as control, was strongly positive for Prx I (Fig. 1h), as it has been described in the literature [25][26][27].…”

“…To verify the possible involvement of the Nrf2-Prx I axis in the synthesis of MMPs in PAC, MMP-2 secretion by PACderived cells was also evaluated. OSCC cells were selected as positive controls, since this aggressive tumor is known to exhibit an increased nuclear expression for Nrf2 [24] and high levels of both Prx I [25][26][27] and MMP-2 [28][29][30][31].…”

Targeting Peroxiredoxin 1 by a Curcumin Analogue, AI-44, Inhibits NLRP3 Inflammasome Activation and Attenuates Lipopolysaccharide-Induced Sepsis in Mice

“…PRDX1 plays an important role in various diseases by involving in many cellular metabolic and signaling processes. In esophageal squamous cell carcinoma, PRDX1 functioned as a tumor suppressor (22), whereas in oral squamous cell carcinoma, PRDX1 was overexpressed and might be a biomarker for the diagnosis and prognosis (23). Additionally, PRDX1 is proven to be essential for antitumor activity of NK cells and antiviral activity of macrophages (24,25).…”

Deregulation of lysophosphatidic acid metabolism in oral cancer promotes cell migration via the up-regulation of COX-2

“…Extracellular LPA is hydrolysed by three plasma membrane bound lipid phosphate phosphatases, LPP1, LPP2 and LPP3 (encoded by the genes PPAP2A, PPAP2C and PPAP2C, respectively), which attenuates downstream signalling, although it is important to note that intracellular functions of LPPs have been described (Tang & Brindley, 2020) COX-2 is a membrane bound enzyme which catalyses the generation of prostanoids, such as prostaglandin E2 (PGE2) (Claria, 2003). Overexpression of COX-2 has been detected in various types of cancer with a number of studies reporting that COX-2 expression levels were significantly higher in OSCCs compared to normal tissue (Byatnal et al, 2015;Goulart Filho et al, 2009;Lee, Kang & Kim, 2015;Moazeni-Roodi et al, 2017;Tang et al, 2003) and overexpression of COX-2 correlated with poor prognosis in cervical SCCs following radiation (Gaffney et al, 2001). In OSCC cells, COX-2 has been shown to mediate αvβ6 integrin-dependent invasion (Nystrom et al, 2006) and is associated with radioresistance (Terakado et al, 2004).…”

“…COX-2 is a membrane bound enzyme which catalyses the generation of prostanoids, such as prostaglandin E2 (PGE2) ( Claria, 2003 ). Overexpression of COX-2 has been detected in various types of cancer with a number of studies reporting that COX-2 expression levels were significantly higher in OSCCs compared to normal tissue ( Byatnal et al, 2015 ; Goulart Filho et al, 2009 ; Lee, Kang & Kim, 2015 ; Moazeni-Roodi et al, 2017 ; Tang et al, 2003 ) and overexpression of COX-2 correlated with poor prognosis in cervical SCCs following radiation ( Gaffney et al, 2001 ). In OSCC cells, COX-2 has been shown to mediate α v β 6 integrin-dependent invasion ( Nystrom et al, 2006 ) and is associated with radioresistance ( Terakado et al, 2004 ).…”