The prognostic value of proliferating cell nuclear antigen (PCNA) and p53 protein expression in patients with advanced nasopharyngeal carcinoma

Wang, Ling‐Feng; Chai, Chee‐Yin; Kuo, Wen‐Rei; Tai, Chih-Feng; Lee, Ka–Wo; Ho, Kuen‐Yao

doi:10.1080/00016480500469545

Cited by 12 publications

(12 citation statements)

References 23 publications

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“…In our study, PCNA expression of severely degenerated tumor cells was clearly inhibited by ALA-PDT, and the less damaged cells showed nearly the same expression level as control cells. PCNA is a cofactor for DNA polymerase ‰, which is required for DNA replication and cell proliferation (17). The surviving tumor cells with unchanged PCNA expression still have relative strong proliferation ability and may contribute to consequent tumor recurrence after ALA-PDT, as indicated by our study.…”

Section: Discussionsupporting

confidence: 54%

“…PCNA is a 36-kDa nuclear polypeptide synthesized during the late G1 to S phase that acts as a homotrimer and helps increase the processivity of leadingstrand synthesis during DNA replication (16). PCNA is also a cofactor for DNA polymerase ‰, which is required for DNA replication and cell proliferation (17). Previous studies have demonstrated that a high level of PCNA expression is associated with poor prognosis in many solid tumors (17,18).…”

Section: Introductionmentioning

confidence: 99%

“…PCNA is also a cofactor for DNA polymerase ‰, which is required for DNA replication and cell proliferation (17). Previous studies have demonstrated that a high level of PCNA expression is associated with poor prognosis in many solid tumors (17,18).…”

Section: Introductionmentioning

confidence: 99%

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Effect of 5-ALA-PDT on VEGF and PCNA expression in human NPC-bearing nude mice

Huang¹

2009

Oncol Rep

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Section: Discussionsupporting

confidence: 54%

Section: Introductionmentioning

confidence: 99%

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Effect of 5-ALA-PDT on VEGF and PCNA expression in human NPC-bearing nude mice

Huang¹

2009

Oncol Rep

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“…RNAi, which is homologous to the gene being suppressed, is the sequence-specific, post-transcriptional gene silencing method caused by small interfering RNA duplexes (siRNAs) and is rapidly being established and holds promise to specifically inhibit gene expression in mammals (20). Based on establishing the CNE2sip53 cell line, which had stable expression of p53 shRNA in CNE2 cell line and satisfactory inhibition of the target p53 protein expression, the effects of persistent down-regulation of p53 gene expression on the transcriptional inactivation of the p53-responsive genes, and on cell proliferation, cell cycle, and the radiation sensitivity and apoptosis after ionizing radiation were demonstrated.…”

Section: Discussionmentioning

confidence: 99%

“…However, experimental evidence has confirmed that the overexpression of p53 seems to occur at an early stage in the development of NPC and associated with advanced disease stage, poor response to therapy. Overexpressed p53 protein is believed to have impaired tumor suppressor activity and to contribute to immortalization and cellular transformation (17,19,20). Until now, the activity of overexpressed p53 in the NPC remains unclear and the role of the p53 in NPC is RNA interference (RNAi) which is a sequence-specific and post-transcriptional gene silencing method initiated by doublestranded RNAs is increasingly being used to specifically inhibit gene expression in mammalian cells (21).…”

Section: Introductionmentioning

confidence: 99%

Functional characterization of p53 in nasopharyngeal carcinoma by stable shRNA expression

Sun

Yi²,

Yang³

et al. 2009

Int J Oncol

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Abstract. Nasopharyngeal carcinoma (NPC) is a highincidence malignancy in Southern China and Southeast Asia. Although mutation of p53 tumor-suppressor gene is a rare event in NPC, NPC has a high frequency of over-expressed/ accumulated p53 protein, which was reported to be dysfunction or inactivation in most of NPC. We report here a functional characterization of p53 in an undifferentiated NPC cell line CNE2. To elucidate the biological function of p53, we employed the RNA interference (RNAi) approach to knockdown the endogenously expressed p53 in CNE2 cells. Interestingly, suppression of p53 expression in CNE2 cells was associated with significant down-regulation of p21 WAF1/CIP1 expression and decreased HDM2 protein level in both steady state and genotoxic stress induced by ionizing radiation (IR). Consistent with these biochemical data were the accelerated cell cycle progression and the increased proliferation rate, suggesting that p53 retained growth inhibitory activity in CNE2 cells. Indeed, down-regulation of p53 in CNE2 enhanced the ability of CNE2 cells to grow anchorage-independently in vitro and to develop tumors in vivo. Together with the radioresistance acquired by CNE2sip53 cells, our data indicate that in contrast to a previous study, p53 in this NPC cell line remains functional, which may have an important therapeutical implication. IntroductionNasopharyngeal carcinoma (NPC) is featured by a remarkable racial and geographic distribution, and is a high-incidence malignancy in Southern China, Southeast Asia, Northern Africa, and Alaska, where the observed incidence rates range from 15 to 50 per 100,000 persons (1-3). NPC can occur in all age groups, but has a bimodal age distribution. The incidence peaks at 50 to 60 years of age; and a small peak is observed during late childhood (3). As an etiologically multi-factorial disease, carcinogenesis of the nasopharynx may result from combined effects of Epstein-Barr viral (EBV), genetic and environmental factors (4-7). Available information on the origin of NPC suggests that genetic alterations of tumor suppressor genes and proto-oncogenes in multiple cellular pathways may be important in multistage NPC carcinogenesis.p53 tumor-suppressor protein plays a pivotal role in regulating cell cycle, differentiation and apoptosis (8). As a transcription factor, p53 can induce the expression of p21 WAF1/CIP1 , which inhibits cyclin-dependent kinases, thereby preventing the phosphorylation of Rb and subsequent cell cycle arrest (9). Mutation of p53 tumor-suppressor gene has been found to be the most frequent genetic alteration in human malignancy. p53 mutations often result in accumulation of the mutant p53 protein, which either loses tumor suppressor function or gains oncogenic activity (10). p53 can also be functionally inactivated by mechanisms other than gene mutation (10). Screen for p53 mutations in the hot-spots for mutation revealed only a low frequency of p53 mutations ranging from 0 to 10%, which might explain the initial high sensitivity observed with ci...

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Viral IL‐10 promotes cell proliferation and cell cycle progression via JAK2/STAT3 signaling pathway in nasopharyngeal carcinoma cells

Ren

Yang

et al. 2020

Biotech and App Biochem

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Epstein–Barr virus (EBV) is positively related to the morbidity of nasopharyngeal carcinoma (NPC) in Asia. After infection, EBV can produce several proteins, including viral interleukin‐10 (vIL‐10). But the mechanism by which vIL‐10 contributes to NPC cell proliferation and cell cycle progression is not well understood. In this study, EBV negative and positive cell lines, and the JAK2/STAT3 signal pathway inhibitor AG490 were used to illustrate the role of vIL‐10 in NPC. Cell proliferation and cell cycle were measured by CCK‐8 and flow cytometry. The expression levels of related protein were measured by Western blotting. High concentrations of vIL‐10 and IL‐6 were found in the EBV positive patients. The expression level of IL‐6 was positively related to the presence of concentration of vIL‐10. vIL‐10 can promote cancer cell proliferation and G1 to S phase transmission via upregulating the IL‐6 protein level by activating the JAK2/STAT3 signal pathway. Furthermore, EBV can induce the formation of cytotoxic T cells, whereas vIL‐10 can block the function of cytotoxic T cells. Taken together, these results suggest that vIL‐10 promotes cell proliferation and cell cycle progression via JAK2/STAT3 signaling pathway in NPC.

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The prognostic value of proliferating cell nuclear antigen (PCNA) and p53 protein expression in patients with advanced nasopharyngeal carcinoma

Cited by 12 publications

References 23 publications

Effect of 5-ALA-PDT on VEGF and PCNA expression in human NPC-bearing nude mice

Effect of 5-ALA-PDT on VEGF and PCNA expression in human NPC-bearing nude mice

Functional characterization of p53 in nasopharyngeal carcinoma by stable shRNA expression

Viral IL‐10 promotes cell proliferation and cell cycle progression via JAK2/STAT3 signaling pathway in nasopharyngeal carcinoma cells

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